Periodontium in health

Periodontium refers to a group of specialized tissues that surround and support the teeth, maintaining them in the maxillary and mandibular bones. The word ‘Periodontium’ is derived from the Greek words peri-, meaning “around” and -odons, meaning “tooth”. Periodontium comprises of root cementum, periodontal ligament, bone lining the tooth socket (alveolar bone), and the part of gingiva facing the tooth surfaces (dentogingival junction).  All of these tooth supporting structures are different in terms of tissue architecture, biochemical and chemical composition. They perform distinct functions and are capable of adapting to the changes in the environment around them. The unique functions that these tissues carry out are,

Attachment: They attach the teeth to their bony housing and also to one another.

Resistance: These tissues resist and resolve the forces produced during mastication, speech, and deglutition.

Adaptation: These tissues have the capability to adapt to the changes in the external environment and wear associated with aging through a continuous process of remodeling and regeneration.

Defense mechanism: They have an internal defense mechanism which protects them against the noxious stimuli present in the oral cavity.

Periodontology is the scientific study of the periodontium in health and in disease 1.  Periodontics is that specialty  of  dentistry  which encompasses  the prevention,  diagnosis,  and treatment of diseases  of the  supporting  and  surrounding  tissues of the  teeth  or their  substitutes;  the  maintenance of the  health,  function  and esthetics of  these structures and tissues;  and  the  replacement  of lost  teeth  and supporting structures by grafting or  implantation  of natural  and  synthetic devices and  materials 1.

A healthy periodontium is required to adequately support the teeth in function. The structural integrity and interactions between the tooth supporting structures are the fundamental requirements for a healthy periodontium. Various disease processes around the teeth result in the destruction of periodontal tissues, thus making them mobile. If the destructive process continues, the tooth/teeth are ultimately lost.

The first step in our journey to understand Periodontology starts with a thorough understanding of the normal periodontium and structures of periodontal tissues in health. In the following discussion, we shall discuss in detail various tooth supporting structures, their development, structural organization, function and their ability to adapt to the changes in the surrounding environment.

Development of orofacial structures

After fertilization of the egg, there occurs a precisely coordinated cascade of developmental processes involving cell migration, growth, differentiation and apoptosis which results in the development of craniofacial structures. During the third week of development, the cranial end of the embryo undergoes precocious development where an oropharyngeal membrane (buccopharyngeal , or oral membrane) is formed at the site of the future face, between the primordium of the heart and the rapidly enlarging primordium of the brain. It is composed of the ectoderm externally and the endoderm internally. During the fourth week of development, this membrane breaks down in order to form the opening between the future oral cavity (primitive mouth or stomodeum) and the foregut.

During the fourth week of development, the cranial region of the human embryo resembles a fish embryo at a comparable stage. The human face begins to form during the 4th week of embryonic development and by the 6th week, the external face is completed. The formation of the external face takes place from two sources: the tissues of the frontonasal process that cover the forebrain (predominantly of neural crest origin); and the tissues of the first (mandibular) pharyngeal arch (mixed mesoderm and neural crest origin). The frontonasal process gives rise to a pair of medial nasal processes (that later contribute to a single globular [intermaxillary] process), and a pair of lateral nasal processes. The mandibular process gives rise to a pair of mandibular processes (actually the pharyngeal arch itself), and a pair of the outgrowths of the arch- the maxillary processes (that later give rise to a pair of palatal processes) (Figure 1.1).

Figure 1.1 Development of orofacial structures

Development of orofacial structures

Development of teeth and periodontium

By the fifth week of development, a horseshoe-shaped band of thickened epithelium (dental lamina) forms on the developing maxillary and mandibular bones. These are essentially the primordial dental arches. Neural crest cells, which are derived from the neural tube play an important role in the development of teeth. These cells are of ectodermal origin migrating into mesenchymal tissue; therefore are also referred to as ectomesenchymal cells.

The dental lamina is comprised of cells that proliferate at a more rapid rate as compared to the adjacent epithelial cells. Later on during development, at predetermined sites on the dental lamina corresponding to ten deciduous teeth, further cellular proliferation takes place forming small protuberances. These protuberances give rise to deciduous teeth. The development of teeth takes place in three distinct phases based on the characteristics of the developing teeth, the bud, bell and cap stages. In the “bud stage” also referred to as primordia of enamel organ, two types of epithelial cells differentiate; one covers the internal surface of the bud (inner epithelium) and the other covers the outer surface of the bud (outer epithelium). Concurrently, there is a marked proliferation of mesenchymal cells facing the inner epithelium of enamel organ which leads to the formation of “dental papilla”.  During this stage, the tooth bud grows around the ectomesenchymal aggregation, taking on the appearance of a cap. This stage of tooth development is referred to as “cap stage”. A condensation of ectomesenchymal cells surrounds the enamel organ and limits the dental papilla which is referred to as “dental sac or follicle”. Eventually, the enamel organ will produce enamel, the dental papilla will produce dentin and pulp, and the dental sac will produce all the supporting structures of a tooth, the periodontium 2.

The “bell stage” is characterized by the formation of two principal hard tissues of the tooth, enamel, and dentin (Figure 1.2a, 1.2b). Enamel is formed by ameloblasts derived from terminal differentiation of cells from the inner epithelium of enamel organ and dentine is formed by odontoblasts derived from mesenchymal cells of the dental papilla. The dental follicle gives rise to cementoblasts, osteoblasts, and fibroblasts which are responsible for the formation of the tooth supporting structures. In the later stages of the bell stage (also referred to as advanced bell stage), the growth of cervical loop cells into the deeper tissues forms Hertwig Epithelial Root Sheath, which determines the root shape of the tooth. The cementoblasts derived from the dental follicle deposit cementum on the root surface and fibroblasts give rise to the periodontal ligament. As the root formation continues, the osteoblasts deposit bone around the root of the tooth. Eventually, mature tooth structure is formed which is supported by supporting tissues, i.e. cementum, periodontal ligament, and bone; invested in the gingiva.

Figure 1.2a Microscopic image of tooth development in advanced bell stage

Advances bell stage

Figure 1.2b Enlaged view of inner epithelium, stellate reticulum and outer enamel epithelium

Advances bell stage

Now, let us discuss in detail the components of the periodontium.


The oral mucosa has been traditionally divided into three categories: lining mucosa, specialized mucosa, and masticatory mucosa. The lining mucosa constitutes about 60% of the total oral mucosa. It is relatively loosely bound to the adjacent structures by the connective tissue that is rich in elastin (Figure 1.3a, 1.3b). It covers the floor of mouth, ventral (underside) tongue, alveolar mucosa, cheeks, lips and soft palate. It does not function during mastication and therefore is non-keratinized, soft and pliable. Specialized mucosa makes around 15% of the total oral mucosa. It covers the dorsal surface of the tongue and composed of cornified epithelial papillae. Masticatory mucosa is the load bearing mucosa during mastication. It is usually keratinized. It constitutes 25% of the total oral mucosa and is present as gingiva (free, attached and interdental) and covers the hard palate.

Figure 1.3a Microscopic image of the oral epithelium demonstrating papillary (P) and reticular (R) part.

Microscopic image of oral epithelium

Figure 1.3b Microscopic image of the oral epithelium demonstrating the basal cells

Basal cells in oral epithelium

Gingiva is that portion of the oral mucosa which covers the tooth-bearing part of the alveolar bone and the cervical neck of the teeth. It is typically coral pink in color, but may vary due to physiologic pigmentation among some races. It exhibits no exudate in periodontal health.

Macroscopic features of gingiva

The gingiva can be anatomically divided into marginal, attached and interdental gingiva (Figure 1.4, 1.5).

Figure 1.4 Macroscopic features of gingiva

Macroscopic features of gingiva

Figure 1.5 Diagrammatic representation of various landmarks of the periodontium

Landmarks of gingiva

 Marginal gingiva:

The marginal gingiva or unattached gingiva forms the coronal border of the gingiva which surrounds the tooth but is not adherent to it. In normal periodontal tissues, it extends approximately 2mm coronal to the CEJ. It is demarcated from the attached gingiva by a shallow linear depression, the free gingival groove in approximately 50% of cases 3. Histologically, the marginal gingiva is made up of oral gingival epithelium coronal to the gingival groove, oral sulcular epithelium, junctional epithelium and subjacent connective tissue of the lamina propria. In the absence of inflammation and pocket formation, the gingival groove runs somewhat parallel to and about 0.5 to 1.5 mm from the gingival margin 4, and it is approximately at the level of the bottom of the gingival sulcus.

Gingival sulcus:

A shallow space between the marginal gingiva and the external tooth surface is termed as gingival sulcus. The boundaries of the gingival sulcus are,

Inner: Tooth surface which may be the enamel, cementum, or a part of each, depending upon the position of the junctional epithelium.

Outer: Sulcular epithelium.

Base: Coronal margin of the attached tissues.

The normal depth of the gingival sulcus and the corresponding width of the marginal gingiva is variable. Under absolutely ideal conditions, the sulcus depth is 0 or close to 0 mm 5. This condition can only be achieved in germ-free animals or after prolonged and stringent plaque control 6, 7. The histological studies have reported the sulcus depth of 1.8 mm in healthy periodontium with a variation of 0-6 mm 8. Others have reported sulcus depth of 1.12 to 2.91 mm 9 and 0.69 mm 10. In general, sulcular depths less than 2 mm to 3 mm in humans and animals are considered as normal 11.  The depth of gingival sulcus is an important indicator of periodontal status. The inflammation in the periodontal tissues due to plaque accumulation results in the conversion of normal sulcus into a pathological pocket. However, it must be remembered that the depth of a sulcus histologically (histological depth) is not necessarily the same as the depth which could be measured with a periodontal probe (clinical depth). Histological sulcus depth is considered as the exact sulcus depth. The sulcus depth determined by probing may be more than the histological depth if the periodontal probe penetrates the connective tissue, especially when it is inflamed or it may be less when the periodontal probe does not reach the bottom of the sulcus.

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Attached gingiva:

The attached gingiva is continuous with the oral epithelium of the free gingiva and is firmly bound to the underlying periosteum of the alveolar bone. It extends from the base of the free gingiva to the mucogingival junction (Figure 1.5) where the keratinized epithelium of attached gingiva abruptly merges with the non-keratinized epithelium of the alveolar mucosa 3. The mucogingival junction is a stable landmark which is probably genetically determined 12. The attached gingiva is usually ‘stippled’, with small regularly spaced depressions on its surface, giving it an “orange peel appearance” 13, 14. It is considered as a sign of healthy gingiva but it must be remembered that the presence or absence of stippling alone cannot determine gingival health 15.

In different areas of the mouth, the width of attached gingiva varies. It is usually greatest in the incisor region (3.5 to 4.5 mm in the maxilla and 3.3 to 3.9 mm in the mandible). In the posterior areas, it is less with the least width in the first premolar area (1.9 mm in the maxilla and 1.8 mm in the mandible) 3. A variation of 1-9 mm in the width of attached gingiva has been reported in humans 16.

In 1972, Lang and Löe16 in a study reported that even when tooth surfaces are kept free of clinically detectable plaque, areas with less than 2 mm of keratinized gingiva (which means less than 1 mm of attached gingiva) remained inflamed with varying amounts of gingival exudate. This persistent inflammation was not found to be related to muscle pulling from frenum insertions. They suggested that an adequate width of keratinized gingiva is important for maintaining the gingival health and advocated the use of various surgical procedures to increase the width of attached gingiva. However, later on, other studies challenged this notion and have suggested that minimizing inflammation is sufficient to maintain attachment levels, even in the absence of “adequate” width of keratinized and attached gingiva 12, 17, 18. In a group of students with a high degree of oral hygiene, it was observed that the areas with inadequate zones of attached gingiva were maintained (4 to 18 years) without further recession 19-21. Another study by Lindhe and Nyman (1980) 22 showed that careful tooth brushing performed daily, monitored for 10-11 years, combined with professional cleaning and polishing of the teeth did not produce further recession of the gingival margin whether or not the gingiva was keratinized.

The mean width of attached gingiva increases from the primary dentition to permanent dentition 23. The anatomical width of attached gingiva increases slightly with the increasing age because of tooth eruption to compensate for occlusal wear 12.

Interdental gingiva:

The interdental gingiva occupies the interproximal spaces between the adjoining teeth (Figure 1.4). The shape of the interdental gingiva is determined by the contact areas of the adjoining teeth and their mesiobuccal, mesiolingual, distobuccal and distolingual line angles. In the anterior teeth, the interdental gingiva assumes the conical shape and is referred to as interdental papilla. Generally, the papillary surface is keratinized. In the posterior teeth, the apex of the interdental gingiva is blunted with buccal and lingual peaks. This shape is referred to as “Col”. Col is a depression between the buccal and lingual papillae which conforms to the interproximal contact area 24. The dimensions of the col are determined by the width of the contact area between adjoining teeth. Because it represents the area of fusion of junctional epithelium of two adjoining teeth, it is non-keratinized and is more susceptible to damage from plaque and other noxious stimuli as compared to the keratinized gingiva.




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Periodontal biotype:

In 1969, Ochsenbein and Ross 25 described two types of gingival forms: flat and highly scalloped. They observed that flat gingival anatomy was found in patients having square teeth while the highly scalloped gingival form was found in patients with a tapered tooth form. Seibert and Lindhe (1989) 26 later used term periodontal biotype to describe gingival forms and classified gingiva as thin scalloped or thick-flat.









Microscopic features of gingiva

Microscopically, the gingiva can be studied under three headings,

  1. Gingival epithelium
  2. Epithelium-connective tissue interface and
  3. Gingival connective tissue.

Gingival epithelium:

The gingival epithelium can be further divided into three functional compartments: outer gingival epithelium, sulcular epithelium, and junctional epithelium.

Outer gingival epithelium:

The outer gingival epithelium consists of keratinized stratified squamous epithelium, which covers the attached gingiva and the crest and outer surface of the marginal gingiva. The principal cells of the gingival epithelium are the keratinocytes. The non-keratinocytes associated with the gingival epithelium are melanocytes, Langerhans cells, and Merkel cells 46-48. The epithelium is organized into four layers which are distinguishable microscopically. These layers are basal cell layer (stratum basale), spinous cell layer (stratum spinosum), granular cell layer (stratum granulosum), and the cornified/keratinized cell layer (stratum corneum).

The basal layer makes the proliferation compartment of the epithelium, whereas the remaining layers make the differentiation compartment. The gingival epithelium is firmly attached to the underlying connective tissue and is non-permeable to water soluble substances. The proliferation of the keratinocytes takes place by mitosis primarily in the basal layer and to some extent in the suprabasal layers. The basal layer consists of one or two layers of cuboidal cells, which are undifferentiated cells. These cells then migrate to the suprabasal layers and differentiate to form mature keratinocytes. A small number of cells remain in the proliferative compartment of the basal layer, participating in the formation of new cells. These are attached to the lamina lucida zone of the basement membrane with hemidesmosomes. The lamina densa zone of the basement membrane faces the connective tissue. Lamina dance consists of anchoring fibers made up of collagen Type VII, which binds to the collagen Type I and III of the extracellular matrix 49, 50.  As the cells move from the basal layer to the surface, they show many biochemical and morphological changes. Morphologically, they become more flattened as they move from basal layer towards the surface.

Stratum spinosum consists of 10-20 layers of cells typically large in size, resembling spines. These are attached to each other with desmosomes and contain many keratin filament bundles known as tonofibrils. In the spinous layer, these cells show numerous contacts via desmosomes which are almost double in number as compared to the cells in the basal layer.

There is a dramatic reduction in cell organelles as the cells move from the basal layer to the stratum granulosum. The nucleus of the cells becomes flattened. Excessive keratohyalin bodies and tonofibrils are seen in the cells. Numerous small electron-dense granules, also known as membrane coating granules or “Odland bodies”, are also observed in the cells of this layer. Odland bodies are small sub-cellular structures of size 200-300 nm. These are modified lysosomes, which contain a large amount of acid phosphatase, an enzyme involved in the destruction of organelle membranes. As the cells move from the stratum granulosum to the stratum corneum, there is a sudden change in the cellular morphology, which involves the destruction of the cell organelle membrane. Thus, these bodies play an important role during keratinization 51-53. In addition to the accumulation of membrane coating granules and keratins, the differentiating keratinocytes synthesize and retain a number of specific proteins, including profilaggrin 54-55, keratolinin,  involucrin 56, and other precursors which are involved in thickening of the cell envelope 57. In the stratified squamous epithelia, the membrane-coating granules are believed to form a superficial, intercellular, permeability barrier. After the extrusion of these granules, the interior of the cell is filled with aggregated cytokeratin filaments, involucrin, loricrin, and other proteins; which are deposited on the inner aspect of the plasma membrane making a thick band of protein which is covalently cross-linked 58, 59. Profilaggrin which is stored in keratohyalin granules of keratinocytes gives rise to filaggrin as these cells move from the stratum granulosum to the stratum corneum. Filaggrin is involved in the formation of the matrix of the most differentiated epithelial cell, the corneocyte.

In the stratum corneum, the cells become flattened and show signs of nucleus disintegration. Two terms, ortho-keratinization and para keratinization are used to describe these changes. Para keratinization is usually observed in the oral gingival epithelium which is characterized by an incomplete disintegration of the nucleus and cytoplasmic organelles. Orthokeratinization is characterized by a complete disintegration of the nucleus and cytoplasmic organelles.  It is found in the skin and may also be seen in the gingival epithelium.  The degree of keratinization of stratum corneum reduces with age and with the onset of menopause 60.

The epithelium is firmly attached to the underlying connective tissue due to a high degree of integration. The basal cells show a large number of hemidesmosomes firmly attaching to the lamina densa of the basal lamina. This integration is further intensified by the presence of numerous serrated keratinocytes and cellular processes (pedicles) of these cells protruding into the connective tissue compartment.

Along with acting as a physical barrier, the gingival epithelium also plays an important role in the innate immune response 61. Research has shown increased expression of integrins 62, intercellular adhesion molecule-1 (ICAM-1) 63, endothelial leukocytes adhesion molecule 1 (ELAM-1) 64, 65 and vascular cell adhesion molecule 1 in the inflamed gingiva 62 . Integrins are heterodimeric glycoproteins, which are involved in the attachment of cells to a large number of extracellular matrix ligands such as laminin, fibronectin, vitronectin, tenascin and osteopontin. It has been demonstrated that expression of integrins especially those functioning as fibronectin receptors is increased in gingival epithelial cells during inflammation 66.  The cell surface adhesion molecules belong to the immunoglobulin class. ICAM-1 molecule interacts with the leukocyte function associated with antigen-1 and is involved in the transmigration of neutrophil through the epithelium. ICAM-1 is expressed by keratinocytes of oral gingival and sulcular epithelium during gingival inflammation and its levels are elevated in periodontitis sites as compared to healthy sites 67. Expression of ELAM-1 by endothelial cells is increased under the influence of cytokines such as TNF-α, IL-1, and bacterial lipopolysaccharides.  It plays an important role in the trans-endothelial migration of leukocytes during inflammation. Its expression has been shown to be increased gingival inflammation 64, 65, 68.

Toll-like receptors are important components of innate immunity. It has been demonstrated that pathogen-associated molecular patterns (PAMPs), shared by many different periodontopathogenic bacteria, stimulate the resident gingival epithelial cells to initiate inflammatory responses in a TLR-dependent manner 69.

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Intercellular junctions:

The intercellular junctions are fundamental to the interactions between cells. They consist of protein complexes which provide contacts between the neighboring cells and the extracellular matrix. The functional classification of cell junctions is as follows,

  • Tight Junctions (Zonula occludens).
  • Adherens Junctions (Zonula adherens).
  • Desmosomes (Macula adherens).
  • Gap Junctions.












Gap Junctions:

These are intercellular channels some 1.5–2 nm in diameter, which permits the free passage of ions and small molecules (up to a molecular weight of about 1000 Daltons) between the cells. They are cylindrical in shape, made up of six copies of transmembrane proteins called connexins. 

Melanocytes, Langerhans cells and Merkel cells in gingiva:


Melanocytes are melanin pigment producing cells. They have protective action against ultraviolet irradiation and have also been shown to be responsive to many immunological mediators 73. They have a protective role due to their ability to interact with active oxygen species (O 2-, H2O2, RO, ROO, etc.) 74. Therefore, epithelial melanin pigmentation provides a defense barrier by acting as a binder of toxic products such as free radicals and polycyclic compounds 75. The distribution of oral melanin pigmentation is about 61% in the hard palate, 22% in the mucous membrane, and 15%  in the tongue76. The melanin pigmentation of the gingiva is normally observed in individuals of African, East-Asian or Hispanic ethnicity 77. Smoking also stimulates melanin production, leading to exceedingly evident intra-oral pigmentation 78, 79. Excessive pigmentation of the gingiva is an esthetic problem and is treated by gingival depigmentation procedures.

Langerhan’s cells:

Dendritic cells are potent antigen-presenting cells and may be the only cells capable of initiating the adaptive immune response. The dendritic cells in the epithelium are known as the Langerhan’s cells. These serve as “sentinels” of the oral mucosa and inform the immune system not only about the entry of the pathogen, but also about the tolerance to self-antigens and commensal microbes. These cells lack desmosomes and tonofilaments. They contain nuclei with clefts, lysosomes, centrioles, Golgi vesicles, a small amount of endoplasmic reticulum, and moderate numbers of mitochondria. A characteristic feature of these cells is the presence of g-specific granules or Birbeck granules (100 nm to 1 μm in size) first described by Birbeck et al. in 1961 80. Some of these granules may be seen associated with the cell membrane. These are rod-shaped and if the terminal vesicle is present, they assume the classic tennis-racket-like shape 81. The exact function of these granules is not clear, however, they have been associated with antigen trapping and presentation.

On the basis of electron microscopic appearance, Langerhan’s cells have been divided into two types,

Type 1: They are pyramidal in shape and are highly dendritic with an electron-lucent cytoplasm. They have numerous Birbeck granules and are usually found in the suprabasal layers.

Type 2:  These are spherical in shape and show fewer dendrites, a more electron-dense cytoplasm with fewer Birbeck granules. They are usually located in the basal layer.

Merkel cells:

Merkel cells, Tactile cells, or Merkel-Ranvier cells are oval-shaped receptor cells found in the deeper layers of the epithelium. These cells have synaptic contacts with somatosensory afferents and are associated with the sense of light touch discrimination 82. These cells are associated with the development of Merkel cell carcinoma (MCC), which is a very aggressive small cell tumor of neuroendocrine origin, usually arising on sun-exposed parts of the skin.

Keratin expression in gingiva:

As the cells move from the basal layer to the cornified layer, their morphological characters change. The keratin expression of gingival epithelium cells changes with their maturation. Keratins are fibrous proteins which take part in cornification of the stratified squamous epithelial tissue. There are 20 keratin polypeptides which have been divided into acidic and basic subfamilies. The gene coding for neutral-basic keratins are found on chromosome 12 (12q13.13), while the acidic carotenes are found on chromosome 17 (17q21.2). The basic to neutral keratins have been numbered from K1 to K8 whereas the acidic keratins have been numbered from K9 to K19. Following expression of keratins is observed in stratified squamous epithelium,

  • All basal cells in stratified epithelia express keratins K5 and K14.
  • K1, K2, K10, and K11 are expressed in the suprabasal layers of keratinized stratified squamous epithelia 83.
  • K4 and K13 expressions are observed in the suprabasal layers of non-keratinized and para keratinized epithelia 84, 85.
  • K6 and K16 are expressed in highly proliferative epithelia.
  • The oral gingival epithelium expresses K5, K14, K1, K2, K10, K11, K6, K8, K16, K18, and K19.
  • The oral sulcular epithelium mostly expresses K5, K14, K4, K13, K6, K16, and K19.
  • Junctional epithelium mostly expresses K5, K14, K13, and K19.
  • Lining mucosa expresses K4/K13 pair which is associated with elasticity, whereas the masticatory mucosa expresses K1/K10 pair which is associated with rigidity.

Renewal of gingival epithelium:

The older cells are continuously replaced by new cells so that the integrity of the tissue can be maintained. In health, the rate of renewal of the epithelial cells equals to the rate of cell exfoliation, so that the total number of the cells remains constant. The renewal time or the turnover time is the time taken for complete renewal of the tissue. In other words, it is the time taken for the exfoliation of a number of cells corresponding to the total number of cells in the tissue, and the formation of the same number of cells through mitotic cell division.

There are a large number of biologically active substances that may stimulate or suppress epithelial cell proliferation. Most of these are peptide growth factors and cytokines. The keratinocyte proliferation is stimulated by epidermal growth factor (EGF), transforming growth factor-α (TGF-α), platelet-derived growth factor (PDGF), and interleukin 1 (IL-1) 86-88. These factors attach to their specific receptors on the cell surface, initiating a cascade of cytoplasmic activities resulting in mitotic cell division 88, 89.  Other factors which affect basal cell mitotic activity are the time of day, stress, and inflammation. The mitotic activity exhibits a 24-hour periodicity, with the highest and lowest rates occurring in the morning and in the evening, respectively 90. Various techniques have been employed to estimate the rate of cell proliferation in different parts of the oral cavity. In general, the rate of cell proliferation is higher for cells in the thin nonkeratinized regions, such as the floor of the mouth and the underside of the tongue as compared to the thicker keratinized regions, such as palate and gingiva 91. The animal studies have demonstrated that mitotic rate in different parts of the oral cavity is in the following descending order: buccal mucosa, hard palate, sulcular epithelium, junctional epithelium, the outer surface of the marginal gingiva, and attached gingiva 90, 92-94. Studies done on humans have estimated that the median cell turnover time on the floor of the mouth is 20 days; buccal mucosa is 14 days and for hard palate is 24 days with mean labeling index of 12.3, 10.2 and 7.2, respectively 89, 91. The mitotic activity of cells changes with age. Researchers have different opinions regarding the change in mitotic activity of the cells with age with some of them believing that it increases with age 94, 95.

Sulcular epithelium:

It is the epithelium which lines the gingival sulcus. Apically, it is bounded by the junctional epithelium and coronally it meets the outer gingival epithelium at the height of the free gingival margin. The sulcular epithelium is similar to the outer gingival epithelium except for the lack of stratum corneum and it does not contain clearly defined stratum granulosum. Hence, this epithelium is non-keratinized. The lack of keratinization makes this area particularly susceptible to influences from micro-organisms. Rete pegs are not present in the sulcular epithelium. The cells of the sulcular epithelium rarely show keratohyalin granules and membrane coating granules. The sulcular epithelium is relatively less impermeable to water soluble substances as compared to junctional epithelium but is more permeable as compared to the oral epithelium.

During gingival inflammation, the sulcular epithelium is densely infiltrated with PMN’s and lymphocytes. Due to infiltration by the immune cells, there is a loss of desmosomal attachment and widening of the intercellular spaces 96, 97.

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Oxygen consumption of gingiva:

In their classical studies Glickman et al. (1949, 1950) 98, 99 estimated the oxygen consumption by normal and healing gingiva using Warburg technique. They concluded that







Junctional epithelium:

The term junctional epithelium denotes the tissue that is affixed to the tooth on one side and to the oral sulcular epithelium and connective tissue on the other side 17, 100. The junctional epithelium is the epithelial component of the dento-gingival unit that is in contact with the tooth surface. It has two distinct basal laminas, the external basal lamina which is continuous with the basal lamina of the sulcular epithelium and attaches the junctional epithelium to the underlying connective tissue and the internal basal lamina that attaches the junctional epithelium to the tooth surface.

It is not keratinized on its free surface layer, so it cannot act as a physical barrier. Hence, other structural and functional characteristics of junctional epithelium must compensate for the absence of this barrier. The junctional epithelium fulfills this difficult task with its special structural framework and the collaboration of its epithelial and non-epithelial cells that provide a very potent antimicrobial mechanism. However, these defense mechanisms do not preclude the development of extensive inflammatory lesions in the gingiva. The conversion of junctional epithelium to pocket epithelium is regarded as the hallmark in the progression of gingivitis to periodontitis. That is why it is a dynamic structural entity and its structure and function differs significantly from the oral gingival epithelium.

General and microscopic features of junctional epithelium include:

  • Its thickness varies from 15-18 cells at the base of the gingival sulcus to 1-2 cells in its most apical portion.
  • Cells are arranged in the base and the suprabasal layers The apical aspect of the junctional epithelium is the site for new cell formation from where cells migrate coronally and desquamate (Figure 1.6).
  • Basal cells and adjacent 1-2 suprabasal layers of cells are cuboidal or slightly spindle-shaped. All remaining cells of the suprabasal layer are flat, oriented parallel to the tooth surface and closely resemble each other. The rate of cell desquamation in the junctional epithelium is greater than that observed in the sulcular epithelium, suggesting its high turnover rate.
  • The innermost layer of suprabasal cells (facing the tooth surface) are called DAT cells (directly attached to the tooth) 101.
  • Lysosomal bodies are found in large numbers in the junctional epithelial cells. The enzymes contained within these lysosomes participate in the eradication of bacteria 102.
  • Junctional epithelial cells have numerous Golgi apparatus, abundant rough endoplasmic reticulum with cisternae and polyribosomes.
  • As already stated, junctional epithelial cells exhibit a unique set of cytokeratins including cytokeratin 5, 13, 14 and 19. Occasionally, the weak activity of cytokeratins 8, 16 and 18 is also seen 103. As compared to other epithelia, junctional epithelial cells are interconnected by a few desmosomes and occasionally by gap junctions 46, 104-106. These features account for the remarkable permeability of the junctional epithelium.
  • A variety of mononuclear leukocytes occupy these interstitial spaces. Neutrophils (PMN’s) are found in the central region of the junctional epithelium and near the tooth surface 50.
  • These mononuclear cells along with their products, products of junctional epithelial cells, blood and tissue fluid represent the first line of defense in the control of the perpetual microbial challenge. These molecules include α- and β-defensins, cathelicidin LL-37, interleukin-8 (IL-8), IL-1 α and -1 β, tumor necrosis factor- α, intercellular adhesion molecule-1, and lymphocyte function antigen-3.
  • Antigen presenting cells (APC’s), Langerhans cells and other dendritic cells are present as well 107.
  • Junctional epithelium, particularly its basal cell layers are well innervated by sensory nerve fibers 108-111.
  • In the absence of clinical signs of inflammation, approximately 30,000 PMN’s migrate per minute from the junctional epithelium of all teeth into the oral cavity 112.
  • Cells originate in the basal layer and migrate in an oblique direction towards and along the tooth surface, where they are sloughed from the free surface.
  • Junctional epithelial cells show no signs of synthesis of membrane coating granules, a finding that agrees with the fact that the junctional epithelium is highly permeable to water soluble substances. The chief barrier to the passage of substances larger than 100 KDa is provided by the external basal lamina.

Figure 1.6 The movement of the cells of junctional epithelium

Movement of cells of junctional epithelium

Formation of Junctional epithelium:

To understand the formation of junctional epithelium, first, we must understand the epithelium- tooth interface. The following concepts have been proposed historically to explain the epithelium-tooth interface.

Gottlieb’s concept

Gottlieb’s experimental and clinical observations led to the concept that the soft tissue of gingiva is organically united to enamel surface 113, 114. He termed the epithelium contacting the tooth surface along with the interface substance as the “epithelial attachment”. According to this concept, after the completion of enamel matrix formation, the ameloblasts finally produce primary enamel cuticle 115. This layer is continuous with the enamel matrix and attaches the cells of REE (reduced enamel epithelium) to the calcified tooth structure.

With the eruption of the tooth, the reduced enamel epithelial cells unite with proliferating oral epithelium. As a result, the epithelial cells adjacent to the enamel surface produce a cornified layer. Gottlieb called this layer as “secondary enamel cuticle”. This layer subsequently becomes separated from the tooth surface, leaving a V-shaped groove, the gingival crevice.

Orban’s concept

Orban and his colleagues gradually modified Gottlieb’s concept in 1944. Orban (1949) 116 incorporated the views of Mayer 117, 118, Beck 119-120 and Weski 121 and proposed that the separation of the epithelial attachment cells from the tooth surface involved preparatory degenerative changes in the epithelium 116. This concept was contradictory to the earlier concept proposed by Gottlieb, which suggested the production of a cornified cuticle layer.

Waerhaugh’s concept

Until 1952, the Gottlieb’s concept of epithelial attachment was quite popular in spite of objections raised against it. In 1952, Waerhaugh presented the concept of “epithelial cuff” 122. This concept was based on the observations made by insertion of thin blades between the surface of the tooth and gingiva.  The blades could be passed apically to the connective tissue attachment at the CEJ without resistance. Based on these findings and other microscopic findings, he concluded that the gingival tissue and tooth are closely adapted but not organically united.

Schroeder and Listgarten’s concept

Resolution of the controversy regarding the nature of the epithelial – tooth interface was not possible until the introduction of transmission electron microscope. In their extensive studies, Schroeder and Listgarten illustrated the details of the structural relationship of epithelial tooth interface 123. They proposed the following terminologies,

Primary epithelial attachment is the term that has been used to describe the relationship of the epithelium to the unerupted tooth. This forms during the maturation of enamel, but prior to tooth eruption. The reduced ameloblasts elaborate a basal lamina referred to as the epithelial attachment lamina. This structure lies in direct contact with the enamel surface and the epithelial cells are attached to it by hemidesmosomes, no evidence indicates the presence of dental cuticle at this stage. As eruption proceeds, mitosis occurs in the basal layer of the oral epithelium and the outer layers of the reduced enamel epithelium, but the ameloblasts no longer divide.

The reduced ameloblasts and other cells of the reduced enamel epithelium are transformed into junctional epithelial cells and the primary enamel epithelial attachment then becomes the secondary epithelial attachment. The ameloblasts do not degenerate or cornify as was previously supposed. They undergo dramatic nuclear and cytoplasmic reorganization, including the development of cytoplasmic filaments, Golgi apparatus and other features that make them indistinguishable from junctional epithelial cells. The secondary epithelial attachment in its simplest form is made up of the epithelial attachment, lamina, and hemidesmosomes.

Near the CEJ, complete enamel may become denuded of its epithelial covering and subsequently may lie in direct contact with the connective tissue. At this site afibrillar cementum is deposited from the cells derived from the connective tissue 124.

Junctional epithelial attachment at molecular level:

The junctional epithelium is an important component of the attachment apparatus facing both the gingival connective tissue and tooth surface. The basement membrane is interposed between the basal cells of the junctional epithelium and gingival connective tissue. Basal lamina forms a part of the interfacial matrix between the tooth facing junctional epithelial cells and tooth surface (DAT cells). At the apical end of the junctional epithelium, basal lamina and basement membrane are continuous.

Basement membrane:

The basement membrane is a thin membranous layer of connective tissue that separates the layer of epithelial cells from the underlying lamina propria. It is an important structural entity which is crucial for compartmentalization (physical barrier function), filtration (selective permeability barrier function), migration, cell polarization, adhesion, and differentiation. Under an electron microscope after heavy metal staining, the basement membrane consists of an electro-dense part, lamina densa, and an electoleucent part, lamina Lucida.  The width of basal lamina is reported to be in the vicinity of 800 A˚ -1200 A˚.

The immunostaining reveals that the basement membrane is composed of collagen Type IV, laminin, heparan sulfate proteoglycan, entactin, and fibronectin. The basement membrane of junctional epithelium resembles other basement membranes, but basal lamina has distinctly different structural and molecular characteristics. It lacks most of the common basement membrane components such as collagen Type IV and VII, most laminin isoforms, perlecans and a lamina fibroreticularis 125-127.Thus, basal lamina of junctional epithelium has its own characteristic features and cannot be regarded as the basement membrane in the true sense.

Expression and functions of molecular factors associated with junctional epithelial cells:

The cell-matrix and cell-cell interactions are mediated by various cellular receptors. In the cellular cytoplasm, these receptors are frequently associated with signaling molecules that respond to the binding of extracellular ligands. Junctional epithelium cells express numerous cell adhesion molecules (CAM’s), such as integrins and cadherins 128. These molecules play an important role during the inflammatory response, facilitating the migration of various cells, which participate in the inflammatory response such as PMN’s, monocytes etc. Following is the general facts about the molecular factors associated with junctional epithelium.

  • Integrins are cell surface receptors that mediate interactions between the cell and extracellular matrix, and also contribute in the cell to cell adhesion 129, 130. The expression of integrins is highest in the basal cell layer.
  • Cadherins are responsible for the tight contacts between cells 128, 131. E-cadherin, an epithelium-specific cell adhesion molecule, plays a crucial role in maintaining the structural integrity of the junctional epithelium.
  • Intercellular adhesion molecule-1 (ICAM-1 or CD-54) on the cellular surface attaches to its ligand lymphocytic function antigen- 3 (LFA-3), facilitating cellular adhesion.
  • α6β4 integrin receptor is expressed by cells in contact with the internal basal lamina.

Role of Intercellular adhesion molecules (ICAM’s) in immunoregulation:

ICAM’s belong to the immunoglobulin receptor family, which facilitate cell-cell interactions in inflammatory reactions. They function as ligands for β2 integrin molecules present on leukocytes and participate in the control of leukocyte migration into inflammatory sites. Intercellular adhesion molecule-1 (ICAM-1) is a critical adhesion molecule for the migration of neutrophils. Expression of ICAM-1 and lymphocyte function antigen-3 (LFA-3) has been demonstrated in the junctional epithelial cells 132-135. The expression of ICAM-1 by the epithelial cells is regulated by pro-inflammatory cytokines such as IL-1 and TNF-α 136, 137.

The high expression of IL-8, a chemotactic cytokine by the junctional epithelial cells is a potent mechanism of PMN migration towards the bacterial challenge. It creates a chemoattractant gradient towards the bottom of the sulcus facilitating routing PMN’s to counter the invading bacteria 135, 138.

Mucosa and junctional epithelium around implants:

The mucus that surrounds an oral implant is not much different from the gingiva around the teeth. Studies done on animal models have analyzed the structural characteristics of the gingiva (around teeth) and the mucosa that encompasses implants 139-144. Their observations were; the healthy, soft, keratinized tissues facing teeth and implants frequently have a pink color and a firm consistency. The two tissues have several microscopic features in common. The gingiva as well as the keratinized, peri-implant mucosa is lined by a well-keratinized oral epithelium that is continuous with the junctional epithelium which is about 2 mm long. The junctional epithelium at a tooth site terminates at the CEJ, apical to which an acellular, extrinsic fiber cementum establishes, which is an important component of the supra-alveolar attachment apparatus. The distance between the CEJ and the bone crest is about 1 mm and is characterized by the presence of collagen fibers that project from the cementum into the connective tissue and the bone. Around an implant with healthy peri-implant tissue, the apical portion of the junctional epithelium is consistently separated from the alveolar bone by a zone of non-inflamed, collagen-rich but cell-poor connective tissue. In the collagen-rich zone, the fibers invest in the marginal bone and run a course more or less parallel to the implant surface. This zone is about 1-1.5 mm high and is continuous with the junctional epithelium. The connective tissue of the peri-implant mucosa can be divided into two zones: the outer and the inner zone. The outer zone is located under the junctional epithelium and is composed of collagen Type I and Type III. In this zone, transformation of collagen fibers takes place. The inner sub-crestal connective tissue zone is primarily composed of collagen Type I and is responsible for mechanical resistance and stability of peri-implant mucosa 145. The total dimension of implant-mucosa attachment is about 3-4 mm. At the biochemical level as well, there are no much difference between the pre-implant and periodontal soft tissue. However, the slightly higher amount of collagen Type V and VI has been noticed in peri-implant soft tissue 145.

The vascular supply of the peri-implant gingival or alveolar mucosa is more limited than that seen around the teeth because of the lack of a periodontal ligament 143. As the principal proprioception in the natural dentition comes from the periodontal ligament; its absence around the implants reduces the tactile sensitivity 146 and reflex function 147.

Regeneration of junctional epithelium:

Injury to junctional epithelium may occur due to intentional or accidental trauma. Usually, it occurs due to accidental trauma during brushing, flossing or eating. Intentional trauma occurs during periodontal surgeries where the junctional epithelium is completely lost. Many studies have been done to investigate the renewal of junctional epithelium. These include studies done on the renewal of junctional epithelium on tooth and implant surface after mechanical detachment by probing, studies done on mechanical trauma during flossing and studies on regeneration of junctional epithelium after gingivectomy procedure which completely removes the junctional epithelium.

A study was done on marmosets in which probing was used to mechanically detach the junctional epithelium. A new and complete attachment, indistinguishable from that in controls was established 5 days after complete separation of the junctional epithelium from the tooth surface 148. Another study done on dental implants revealed that healing around the implants takes almost the same time for re-establishment of junctional epithelium as that around the tooth 149. Both of the above studies showed that probing injury is a completely reversible injury to the junctional epithelium.


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Turnover of the attachment epithelium:

One study investigated renewal time in the gingival epithelium of marmosets using injections of tritiated thymidine and autoradiography. Epithelial cells in the attached gingiva exhibited a renewal rate of 10.4 days, whereas the corresponding rate for the epithelial cuff was 5.8 days 157. In another study, autoradiography was used to study the rate of migration of attachment epithelium. The authors observed that the rate was comparable to the rate of tooth eruption, suggesting that the location of the attachment is relatively stable 92.

Epithelium-connective tissue interface:

As already stated, there is a firm attachment of the epithelium to the underlying connective tissue in the attached gingiva. The epithelial rete pegs project deep into the connective tissue. Similarly, there are deep connective tissue papillae projections into a more or less uniform sheet of epithelium. This high degree of interdigitation between epithelium and connective tissue is clinically observed as stippling on the epithelial surface.

The basement membrane zone provides attachment of the epithelium to the underlying connective tissue. Basal lamina which is a component of the basement membrane acts as a solid, intact sheet restricting the passage of water soluble substances, except for the passage of the PMN’s and lymphocytes during inflammation. In various forms of desquamative gingivitis such as bullous mucosal lesions, autoantibodies are directed against the cementing molecules in the basement membrane zone, resulting in the epithelium-connective tissue split.

The gingival basal lamina plays an important role in the survival of the epithelium by allowing the nutritional and gaseous exchange between the connective tissue and epithelium. During surgical procedures such as free gingival graft, the survival of the grafted tissue depends on the diffusion of nutrients through this membrane.

Gingival connective tissue:

The connective tissue of the gingiva is termed as lamina propria. It is densely collagenous with a few elastic fibers. It consists of two layers: papillary and reticular layer. The papillary layer lies adjacent to the epithelium and the reticular layer is contiguous with the periosteum of the alveolar bone. In the papillary layer of connective tissue, papillary projections interdigitating with epithelial rete pegs can be seen. Densely packed collagen fibers can be seen in the connective tissue with specific orientations and attachments. Other important components of gingival connective tissue are various cells and macromolecules. Following is the detailed description of these components,

Gingival fibers:

There is a specific orientation and organization of the collagen fiber bundles in the gingival connective tissue, also referred to as fiber apparatus of the gingiva. These fiber bundles have been named according to their location, origin and insertion as dentogingival, alveologingival, periosteogingival, circular, semicircular, transgingival, intergingival, intercircular, transseptal and interpapillary groups 158-160.

Figure 1.7 a,b Various gingival fibers

Gingival fibers a


Gingival fibers b


Dentogingival fibers:

These fibers are embedded in the cementum near the cementoenamel junction (CEJ) and fan out into the gingival connective tissue attaching gingiva to the teeth (Figure 1.7a, 1.7b).

Alveologingival fibers:

These fibers extend from the periosteum of the alveolar crest into the gingival connective tissue. These fiber bundles attach the gingiva to the bone.

Periosteogingival fibers:

These fibers extend laterally from the periosteum of the alveolar bone. They attach the gingiva to the bone.

Circular fibers:

These fibers encircle the tooth in a ring-like manner coronal to the alveolar crest connecting adjacent teeth to one another.  These fibers are not attached to the cementum of the tooth.

Semicircular fibers:

The fibers emanate from cementum near the CEJ, cross the free marginal gingiva, and insert into a similar position on the opposite side of the tooth.

Transgingival fibers:

These fibers extend from the cementum near the CEJ of teeth and run horizontally between adjacent teeth, linking them into a dental arch unit.

Intergingival fibers:

These fibers extend in a mesiodistal direction along the entire dental arch and around the last molars in the arch. In this way, they link adjacent teeth into a dental arch unit.

Intercircular fibers:

These fibers encircle several teeth in the arch linking adjacent teeth into a dental arch unit.

Transseptal fibers:

These fibers pass from the cementum of one tooth, over the crest of alveolar bone to the cementum of the adjacent tooth. They connect adjacent teeth to one another and secure their alignment in the arch.

Interpapillary fibers:

These fibers are located coronal to the transseptal fibers connecting the oral and vestibular interdental papillae of posterior teeth.

Cellular components of gingival connective tissue:

There is a variety of resident cells in the gingival connective tissue, making around 8% of its total volume. Fibroblasts are the primary cellular element of the gingival connective tissue, responsible for the formation and degradation of the collagen fibers. They play an important role during healing after the periodontal surgery. Other cells, which can be seen in the gingival connective tissue are macrophages, mast cells, lymphoid cells and blood leukocytes. Following is the detailed description of the cellular components of gingival connective tissue,


Gingival fibroblasts are the most abundant cells in the periodontal connective tissue. They make around 65% of the total cell volume of the gingival connective tissue. According to their functional state, they exhibit considerable variation in their morphology, size, and shape. They are spindle-shaped or stellate-shaped cells (active fibroblasts) with centrally placed oval or round nucleus. These cells produce extracellular matrix products, i.e. collagen fibers and amorphous ground substance, thus playing an important role in the formation of extracellular matrix. Fibroblasts are also responsible for the resorption of collagen fibers, thus playing an important role in collagen homeostasis. Present evidence suggests a considerable heterogenecity in the fibroblast cell populations 161.

When observed under an electron microscope, these cells demonstrate abundant mitochondria, a prominent Golgi apparatus and densely packed lamellae of rough endoplasmic reticulum, suggestive of active synthetic cells. The fibroblast activity is controlled by local cellular environment, both the extracellular matrix, and soluble factors.

Polymorphonuclear cells (PMN’s):

These are primary cells which are abundantly found in an acute inflammatory reaction. These cells are commonly found in the junctional epithelium where they travel along the chemoattractant gradient to reach the site of bacterial accumulation. Under the influence of various pro-inflammatory mediators, these cells migrate out of the blood vessels by trans-endothelial migration to reach the site of insult. Under healthy conditions when there is no inflammation, these cells are rarely found in the gingival connective tissue.

Lymphocytes and plasma cells:

Lymphocytes and plasma cells are the key cells involved in the immune response against infection. Most of the lymphocytes found in gingiva are T-lymphocytes, which are primarily present in the zone immediately adjacent to the junctional epithelium. These constitute the cell-mediated immune response against infection. The humoral response or the antibody-mediated response is generated through plasma cells, which are derived from mature B-cells. The mature B-cells exhibit a high nucleus to cytoplasm ratio, little rough endoplasmic reticulum (RER), and an uncondensed nucleus. In contrast, plasma cells exhibit a small, dense, eccentric nucleus, voluminous cytoplasm containing prominent amounts of RER and enlarged Golgi apparatus. Plasma cells have a basophilic cytoplasm and an eccentric nucleus which is heterochromatin in a characteristic cartwheel or clock face arrangement.

Plasma cells are present predominantly around the gingival blood vessels. During early lesion in periodontal inflammation, the predominant cells are primarily T-lymphocytes. As the lesion becomes chronic, more number of plasma cells and mature B-cells can be seen in the inflamed periodontal tissue.

Monocytes and macrophages:

Monocytes and macrophages are mononuclear phagocytes that play an important role in tissue homeostasis and immunity. Monocytes circulate in the blood, bone marrow, and spleen and do not proliferate in a steady state. These cells possess chemokine receptors and pathogen recognition receptors that mediate their migration from blood to tissues during infection. Macrophages are resident phagocytic cells in lymphoid and non-lymphoid tissues. These cells are characterized by the presence of relatively small oval or indented nucleus, abundant cytoplasm containing primary and secondary lysosomes, microfilaments, scattered rough endoplasmic reticulum and numerous small vesicles distributed in the cytoplasm. Usually, only a small population of these cells is present in the normal non-inflamed gingiva. During inflammation, there is an increase in the number of these cells in the gingival connective tissue.

Mast cells:

Mast cells are large granular cells that arise from multipotent precursors in the bone marrow and are normally distributed throughout the connective tissues 162. These cells are involved in numerous activities ranging from control of vasculature to tissue injury and repair, allergic inflammation and host defense. These cells are located near blood vessels or nerve endings where they release their products on stimulation. Their products include heparin, histamine and large variety of other pro-inflammatory mediators, including interleukins IL-1, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, and IL-16, together with granulocyte-macrophage colony stimulating factor (GM-CSF), platelet-activating factor (PAF), RANTES, macrophage inflammatory protein (MIP-1a), and the arachidonic acid metabolites prostaglandin 2 and leukotriene C4 163. It has been demonstrated that in inflamed and healing gingiva, the number of mast cells increases 164.

The cell membrane of mast cells possesses a relatively large spectrum of receptors capable of mediating the interaction with components of the immune system, thus playing an important role in immune response. They are also an important source of growth factors, such as vascular endothelial growth factor or nerve growth factor.

Osteoblasts and osteoclasts:

These cells are found close to the alveolar process and are responsible for the bone formation and resorption respectively (described later).

Cementoblasts and cementoclasts:

These cells are responsible for the formation and resorption of cementum respectively (described later).

Macromolecular components of gingival connective tissue:

The gingival connective tissue contains collagen and non-collagenous glycoproteins. The non-collagenous glycoproteins include laminin, fibronectin, proteoglycans, a small quantity of elastin and serum components.


It is the most abundant protein in the connective tissue. The characteristic feature of collagen is its balanced structure. Collagen molecules are synthesized by resident fibroblasts.  To date, there are 28 known collagen types in mammals, which form triple helices through three polypeptide chains winding around each other in a rope-like structure 165, 166. The triple helical structure is formed due to the presence of Glycine (Gly) at every third position in the amino acid chain. Hence, the collagenous domain has the repeated sequence X-Y-Gly [where X and Y can be any amino acid, but one of them is often a proline (Pro)]. All different forms of collagen cannot form fibrils. Those which can form fibrils include collagen Types I, II, III, V, XI, XXIV, and XXVII. In gingiva, the collagen accounts for 60% of the total tissue protein 167. Collagen Type I and Type III make the majority of the extractable collagen from gingival tissue accounting for around 99%. Collagen Type V accounts for less than 1% 168.

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Collagen synthesis:

There are more than 20 forms of collagen found in our body out of which collagen Type I is the most abundant. They are encoded by different genes. The triple helical structure of collagen is made up of three very long protein chains. Each protein chain is referred to as “α” chain. Two of the α chains are identical and are called α-1 chains, whereas the third chain is slightly different and is called α-2. The triple helical structure made of these three chains is called as collagen monomer. Most of the collagens have a triple helical structure. However, a few types of collagen have slightly different amino acid compositions and perform other specific functions. For example, collagen Type II is usually associated with proteoglycans or “ground substance” and therefore functions as a shock absorber. Collagen Type III is an important component of blood vessel walls and skin. It provides flexibility to the blood vessels and plays an important role during early wound healing. Collagen Type IV is an important component of basement membranes and basal lamina structures and functions as a filtration system.












The turnover rate of collagen is higher in oral connective tissue than in skin and bone. In a study where radioautographic technique was used, it was observed that the rate of incorporation of labeled proline in periodontal collagen was high 179. In another study on guinea pigs, it was observed that the incorporation of labeled proline and its hydroxylation in oral connective tissue was higher than skin 180.  Many other researchers have supported these findings 181-186. The collagen in the gingiva is different in various aspects from that in the skin. Most importantly, 3-hydroxyproline which is present in the skin collagen is not found in gingival or edentulous ridge connective tissue. Another difference is that collagen Type I and III in gingiva have significantly less 4-hydroxyproline and more hydroxylysine than those isolated from the skin 187.


Laminins are heterotrimeric proteins of the extracellular matrix that are composed of α-, β- and γ-subunits. There are multiple isoforms of each subunit yielding a variety (15) of laminin proteins cataloged to date. It binds to cell surface receptors as well as various matrix components. It is an important component of basal lamina due to its property to form fibrils and networks itself, as well as with collagen Type IV.


Fibronectin is a ubiquitous and essential component of the extracellular matrix (ECM). It is also an important component of plasma for its role in thrombosis. The name “fibronectin” is derived from the Latin words fibra, meaning fiber, and nectere, meaning to bind. Fibronectin is formed by the joining of two similar polypeptide subunits via a pair of disulfide bonds near the C-terminal of each. It contains two major heparin-binding domains that interact with heparan sulfate proteoglycans. It also contains collagen as well as fibrin-binding sites.

Cellular fibronectin is secreted by fibroblasts and multiple other cell types and is organized into fibrils contributing to the insoluble extracellular matrix. Fibronectin binds to many receptors of the integrin family. Along with this, it has a remarkably wide variety of functional activities. Besides binding to the cell surfaces through integrins, It also binds to a number of biologically important molecules that include heparin, collagen/gelatin, and fibrin. It plays an important role during wound healing. It facilitates spreading of platelets on the collagen fibers, their binding to fibrin clot, promoting opsonisation by phagocytic cells and promoting migration of fibroblasts. It has specific domains for binding proteoglycans, which make it an important binding material in the extracellular matrix.


Proteoglycans are the proteins that are heavily glycosylated. Structurally, these are formed of glycosaminoglycans (GAGs) covalently attached to the core proteins. They constitute a major component of the extracellular matrix. An important function of proteoglycans in the extracellular matrix is to provide resilience and resistance to compression under pressure, which is due to their high degree of supramolecular organization. The biosynthesis of proteoglycans require several modifying enzymes in addition to glycosyltransferases. These can be classified on the basis of the nature of their glycosaminoglycan chains (Table 1.1).

Table 1.1

Classification of proteoglycans based on the nature of their glycosaminoglycan chains 

Glycosaminoglycan chain
Small proteoglycans
Large proteoglycans
Chondroitin sulfate/
Dermatan sulfate
Decorin, kDa=36
Biglycan, kDa=38
Versican, kDa=260-370
Heparan sulfate /
chondroitin sulfate
Testican, kDa=44Perlecan, kDa=400-470
Chondroitin sulfateBikunin, 25 kDaNeurocan, kDa=136
Aggrecan, kDa=220,
Keratan sulfateFibromodulin, kDa=42
Lumican, kDa=38

The protein part of the proteoglycans is synthesized by ribosomes and then it enters the lumen of the rough endoplasmic reticulum. The glycosylation of the proteoglycan occurs in the Golgi apparatus in multiple enzymatic steps. A tetrasaccharide link is then attached to a serine side chain on the core protein to serve as a primer for polysaccharide growth. Sugar units are then added to this structure in the presence of enzyme glycosyl transferase. The completely formed proteoglycans are then exported to extracellular matrix space by secretory vesicles.

In gingival tissue, dermatan sulfate is the predominant glycosaminoglycan accounting up to 60% of the total. The remaining components include hyaluronic acid, heparan sulfate and chondroitin sulfate 188, 189. Initially, proteoglycans were considered as an inert cementing substance, but now it is clear that because of their charged nature, they are highly hydrated and are capable of interacting with a wide variety of matrix and cell surface components, which is vital for the maintenance of normal tissue function.


Elastin is another important structural protein found in the extracellular matrix (ECM) of gingival connective tissue. The elastin formation, also known as elastogenesis, takes place through the assembly and cross-linking of the protein tropoelastin. As discussed in the synthesis of collagen, the expression of genes encoding for elastin result in the formation of tropoelastin. The tropoelastin inside the cell, then associates with the elastin binding protein (EBP) and this complex is secreted to the cell surface. The elastin binding protein (EBP) then dissociates from the tropoelastin molecule and re-enters the cell. The interchain covalent crosslinking system present in elastin is similar to that of collagen. Tropoelastin aggregates are oxidized by lysyl oxidase leading to cross-linked elastin.

Elastin plays a key structural role in elastic tissues, including arteries, skin, ligament, cartilage and tendons where it is found in high concentrations 190. It is present in the connective tissue of oral mucosa and attached gingiva. A limited content of elastin is present in the periodontal ligament.

Vascular supply of gingiva:

There is a network of blood vessels which supply and drain teeth and their supporting tissues. These are as follows,

Arterial supply of mandibular and maxillary gingiva:

The mandibular teeth and their supporting structures are supplied by branches of inferior alveolar (dental) artery, including mental, sublingual and buccal arteries. The inferior alveolar artery is a branch of the internal maxillary artery. Near its origin, the inferior alveolar artery has a lingual branch which supplies the tongue and adjacent mucous membrane. The inferior alveolar artery descends posterior to the inferior alveolar nerve to enter the mandibular foramen. Before entering the foramen it gives off a mylohyoid branch, which pierces the sphenomandibular ligament and descends with the mylohyoid nerve to supply the mylohyoid muscle. The inferior alveolar artery then traverses the mandibular canal with the inferior alveolar nerves and divides into mental and incisor branches near the first premolar. The mental branch leaves the mental foramen and supplies the chin and anastomoses with submental and inferior labial arteries. The incisor branch continues below the incisor till the midline where it anastomoses with the artery of the opposite side. During its course in the bone, the inferior alveolar artery gives off a series of branches corresponding to the number of roots of the teeth and a few branches which are lost in the cancellous tissue.

The arterial supply of the maxillary teeth and their supporting structures is by the posterior superior alveolar artery, infraorbital artery, the greater palatine artery and the sphenopalatine arteries. The posterior superior alveolar artery gives branches over the maxillary tuberosity supplying the maxillary teeth in the molar region, alveolar bone and the mucosa. These branches anastomose with the branches of the facial artery. The anterior superior alveolar artery, which is a branch of the infraorbital artery, curves through the canalis sinuosus following the rim of the anterior nasal aperture supplies the anterior teeth in the canine and incisor region. On the palatal aspect, the greater palatine artery supplies the palatal gingiva. In the anterior region the nasopalatine artery supplies the palatal gingiva.

The gingiva receives its arterial supply mainly from three sources: the supraperiosteal arterioles, the vessels from the periodontal ligament and arterioles emerging from the crest of the interdental septa. Out of these three sources, the gingiva is primarily supplied by the periosteal arterioles that course over the alveolar process. These arterioles supply a capillary plexus that course below the gingival epithelia. They form anastomoses with capillaries from the periodontal ligament and alveolar bone 191, 192. Fine capillary loops can be seen extending into the papillary layer of the epithelium from the capillary plexus 193. The approximate diameter of the blood vessels in this plexus is 40 μm, indicating that these are mainly venules.  The capillary plexus beneath the junctional epithelium lacks distinct capillary loops 97, 194, 195. However, during inflammation, these capillaries enlarge and acquire varicosities 196, 197. These capillaries subjacent to the junctional epithelium are a major source of the gingival crevicular fluid and the inflammatory cells that migrate into the lamina propria and then into the junctional epithelium during inflammation 198, 199.

Venous and lymphatic drainage:

The venous and the lymphatic drainage of gingiva is closely associated with the arterial supply. In the maxilla, the gingival lymphatic vessels drain into the deep cervical lymph nodes. In the mandible, they drain into the mental, submandibular and the cervical lymph nodes. These lymphatic vessels return the fluid and filterable plasma components to the blood via thoracic duct.

Innervation of the gingiva:

The gingiva in various regions of the oral cavity is supplied by the second and the third division of the trigeminal nerve. The nerve supply of gingiva follows the course of vascular supply. In the maxilla, the gingiva is supplied by the posterior, middle and the anterior superior alveolar nerve, branches of the infraorbital nerve, the greater palatine nerve, and nasopalatine nerve. The middle superior alveolar nerve is present in around 80% of individuals. The buccal nerve supplies variably in the buccal molar region.

In the mandible, the gingiva is largely supplied by the inferior alveolar nerve. The buccal nerve supplies buccal gingiva in relation to the molars and premolars. The branches of the lingual nerve supply the gingiva on the lingual aspect of all lower teeth. Most of the nerve endings in gingiva terminate within the lamina propria. Only a few nerve endings are present in the epithelium. Various neural terminal endings present in gingiva include Meissner corpuscles, Krause type end bulbs, and encapsulated spindles.

Normal clinical features of gingiva and their correlation with the microscopic features

Various clinical features of normal gingiva can be co-related to the microscopic findings. These are,


The color of the normal gingiva is pale or coral pink. There are four factors which determine the color of the gingiva. These are vascular supply, the thickness of the epithelium, the degree of keratinization and physiologic pigmentation. During chronic inflammation, the gingiva may appear reddish pink/bluish in color, whereas during acute inflammation it may appear bright red in color. These changes during inflammation are because of increased blood flow, increased permeability of capillaries, and increased collection of defense cells and tissue fluid. The color of healthy gingiva is different from the alveolar mucosa which is red in color. Also, the alveolar mucosa is smooth and shiny rather than stippled as seen in attached gingiva. The thickness of the epithelium also affects the color of the gingiva. It varies from individual to individual. As discussed earlier, there are two types of periodontal biotypes: thin and thick.

Pigmentation in gingiva is produced by melanin producing cells, the melanocytes. The melanin pigmentation of the gingiva varies with the race and complexion. It is lighter in blond individuals with a fair complexion as compared to the dark-complexioned individuals. The gingival pigmentation is minimal in Caucasian individuals, whereas African and Asian individuals have brown or bluish-black areas of pigmentation.

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Effect of subgingival restorations on gingival color:

The thickness of the gingiva affects the gingival color when various restorative materials are placed under gingival margins. In a study done by Jung et al. (2007) 200, various materials,






Surface texture:

As already stated, the surface of attached gingiva is stippled, demonstrating an ‘orange peel appearance’. Stippling is present on the attached gingiva and interdental papillae. It should be viewed under broad daylight and not the dental chair light, after drying the gingiva with cotton. This is because dental chair light is focused, whereas the broad daylight comes from all directions, thus making stippling more visible. It is usually absent in children less than 5 years of age and in elderly individuals. It is more prominent on the labial surface as compared to lingual surface and may be absent in some individuals.

Histologically, stippling corresponds to the epithelial and connective tissue inter-digitations. The rete ridges and rete peg arrangement between 123

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The normal contour of the gingiva is scalloped. The attached gingiva has a festooned appearance with intermittent prominences corresponding to the root surface contour. The contour of the gingiva depends on the shape and the alignment of the teeth in the dental arch. When teeth are more labially placed, the contour of the gingiva becomes accentuated and when teeth and more lingually placed, the contour of the gingiva becomes more horizontally flattened. Along with this, the position and size of the contact area and dimensions of the embrasures also determine the gingival contour.


The shape of the interdental papilla is determined by the location and shape of the interproximal contact and contour of the proximal tooth surfaces. In anterior teeth, the interdental papilla is pyramidal-shaped, whereas in the posterior teeth, it is flat or saddle-shaped.


The size of the gingiva refers to the sum total of the cellular and connective tissue components of the gingiva. Change in the size of gingiva is associated with pathological conditions. For example, in the case of gingival enlargement the connective tissue component of the gingiva is increased.


The consistency of the normal gingiva is firm and resilient. The gingiva is palpated with a blunt instrument to check for its consistency. The gingival connective tissue is composed of collagen fibers and is firmly bound to the underlying mucoperiosteum, giving it a firm and resilient consistency. During gingival inflammation, the gingival consistency becomes soft and edematous. This is because of the increased vascular flow, increased vascular permeability, and fluid accumulation.

Periodontal ligament (PDL)


The periodontal ligament is derived from the dental sac tissue, which invests the tooth germ. It is a complex, vascular, and highly cellular soft connective tissue interposed between roots of the teeth and the inner wall of the alveolar socket. It has the shape of an “hour glass” and is narrowest at the mid-root level. The PDL consists of a fibrous stroma in a gel of ground substance containing cells, blood vessels and nerves 202. Many terms have been used previously to describe periodontal ligament, including desmondont, gomphosis, pericementum, dental periosteum, alveolodental ligament and periodontal membrane. It has a rapid turnover rate and high remodeling capacity because of which it has the ability to adapt and maintain a constant width despite being exposed to rapidly changing physical forces such as mastication, speech and orthodontic tooth movement 203, 204. Also, PDL has a remarkable capacity for renewal and repair, playing a pivotal role in periodontal regeneration. Major functions of PDL are supportive, sensory, nutritive, and remodeling.

Development of periodontal ligament

At the onset of PDL formation, the PDL space is filled with unrecognized connective tissue. The first step in the formation of PDL is the formation of fringe fibers, which are newly synthesized nascent fiber bundles. These fibers are formed on the newly formed root dentine and along the bone surfaces and are deposited by elongated, highly polarized fibroblasts. These fibers are tightly packed with the deposition of acellular extrinsic fiber cementum by cementoblasts. As the tooth erupts, these fringe fibers merge across the width of the periodontal ligament and make the Principal fiber bundles of PDL. These fiber bundles become embedded on one side in cementum and on the other side in alveolar bone and are referred to as Sharpey’s fibers. The orientation of these fibers changes with the eruption of the tooth. Initially, before tooth eruption the CEJ is below the alveolar crest. So, the PDL fibers are oriented obliquely. As the tooth erupts, the CEJ coincides with alveolar crest. So, just below the free gingival fibers oblique fibers become horizontally aligned (alveolar crest fibers). The middle zone of the PDL is formed of collagen fiber splicing and unsplicing designed to accommodate minor tooth movements. This area is referred to as intermediate plexus.

Along with the PDL fibers which make up to 70% of the total volume of PDL, the remaining 30% is occupied by the dense connective tissue, which is composed of blood vessels, lymphatic vessels, and nerve fibers (Table 1.2). The inflammatory cells can be seen in the perivascular spaces, the number of which increases during inflammation. Garant (2003) 205 has subdivided periodontal ligament into three regions,

  1. A bone-related region, rich in cells and blood vessels.
  2. A cementum-related region, characterized by dense, well-ordered collagen bundles.
  3. A middle zone containing fewer cells and thinner collagen fibrils.

Table 1.2

Composition of periodontal ligament


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Components of PDL

Structurally, human PDL consists of collagen fibers (53-57%), blood vessels and nerve endings (1-2%) that are embedded in an amorphous mucopolysaccharide matrix 207.

Periodontal ligament fibers:

The fibers in PDL tissue mainly comprise of collagen and elastic fibers. The principal fibers of the PDL are primarily composed of collagen Type I and Type III. Collagen Type III is known as fetal collagen and is important in the early phases of wound healing. Other collagens such as Types VI and XII are also present in PDL but in less quantity 208, 209. The principal fibers have distinct collagen fiber bundles with their terminal ends inserting into the cementum and alveolar bone (Sharpey’s fibers) (Figure 1.8). The principal fibers inserted into the bone are widely separated as compared to those inserted into cementum. Also, they are fewer in number and widely separated as compared to those entering the cementum 210-212. The diameter of these fiber bundles varies from 1-4 μm. Three-dimensionally, the path of these fibers from the cementum to the bone is not just radial but may also be tangential. Furthermore, these fibers may cross each other, thus providing reinforcement to one another.

Figure 1.8 The microscopic section of tooth demonstrating periodontal ligament


The Sharpey’s fibers present on the distal root surfaces are longer with distinct appositional lines in the alveolar bone as compared to the mesial surface of the root. This is because the teeth move in a mesial direction throughout life. So, there is continued deposition of bone opposite to the distal root surface as compared to the mesial root surface where it is resorbed and deposited in alternate cycles. It creates scalloped “reversal lines” in the alveolar bone

Along with the principal fibers which run from the cementum to the bone, there are also fibers which run parallel to the root surface, designated as “indifferent fiber plexus” 213, 214. These fibers are primarily seen in the apical half of the root. These fibers may also get incorporated into the mineralized matrix of bone or cementum, like the Sharpey’s fibers.

According to Sloan and Carter 215, the PDL fibers are arranged in following distinct groups of principal fibers (Figure 1.9),

Figure 1.8 The arrangement of distinct group of fibers in periodontal ligament

Distinct groups of periodontal ligament fibers

(1-crestal, 2-horizontal, 3-oblique, 4-apical, 5-trans-septal, 6-inter-radicular)

Dentogingival fibers:

These fibers run outwards from the tooth surface into the gingival connective tissue.

Alveolar crest group:

These fibers are inserted into the cementum and alveolar crest apical to the junctional epithelium. They function to retain the tooth in the socket by countering the coronal thrust. These fibers also resist the lateral movement of the tooth.

Horizontal group:

These fibers insert at right angles into the cementum and alveolar bone. Their function is same as that of the alveolar crest group.

Oblique group:


Apical group:

These fibers radiate in an irregular fashion and connect the apical aspect of the root to the bone at the fundus of the socket. They are not present on the incompletely formed roots. These fibers prevent tooth tipping and resist forces of luxation. These fibers also protect the neuro-vasculature at the root apex.

Transseptal fibers:

These are interproximal fibers which insert into the cementum of adjacent teeth. They are a constant finding and will undergo reconstruction even when alveolar bone loss has occurred from periodontal disease. These fibers may be considered to belong to the gingival tissue because they do not have an osseous attachment 216.

Interradicular fibers:

These fibers are found only between the roots of multi-rooted teeth. These fiber bundles course over the crest of the interradicular septum in the furcation area of these teeth. These fibers function to resist tipping of tooth, forces of luxation and rotation.

Other than collagen fibers, elastic fibers (Oxytalan and Elaunin) are also present in PDL. These fibers can be demonstrated with elastin stains in light microscope 217. Oxytalan fibers, run vertically along the cementum surface of the apical root and form a three-dimensional branching network around the root 218. These fibers have been thought to regulate the vascular flow 219. Fibrillin-1 and elastin are the components of oxytalan fibers, but in the human periodontal ligament, only Fibrillin-1 is present 220, 221.

These fibers may be considered as a separate type of connective tissue elements because they may be easily distinguished histologically from other connective tissue elements including collagen 222. They measure between 0.2 and 1.5 µm in diameter when seen under the electron microscope and have been reported to occupy 3% of the PDL in humans 223. Oxytalan fibers are widely distributed in the ligament whereas elaunin fibers are limited mainly to the apical region of the ligament in close association with the blood vessels. The presence of elaunin fibers in the apical areas of the root in PDL has been associated with increased mechanical stresses in these areas as compared to other areas of the root 224.

Cellular components of periodontal ligament:

There are a variety of cells present in PDL involved in the maintenance of its normal structural organization, including osteoblasts, osteoclasts, fibroblasts, epithelial cell rests of Malassez, monocytes, macrophages, undifferentiated mesenchymal cells, cementoblasts and odontoclasts. These cells are involved in constant remodeling of the PDL, cementum, and alveolar bone.


Principal cells involved in PDL homeostasis and regeneration are fibroblasts 225. Unlike the gingival fibroblasts which are derived from the general mesenchyme, the PDL fibroblasts are ecto-mesenchymal in origin 226. Structurally, the fibroblasts are spindle-shaped with an elongated appearance in vitro 227. In vivo, fibroblasts demonstrate an irregular disc-shape with a mean diameter of about 30 µm 228. These cells demonstrate all the features of an actively synthesizing cell such as abundant rough endoplasmic reticulum, mitochondria, Golgi complex, and vesicles. In PDL, the fibroblasts are oriented parallel to the ligament fiber bundles and they wrap around them with their cytoplasmic processes 229. When stained with colloidal silver, they demonstrate either one or two regions of acidic proteins which are associated with nucleolar organizer regions. The PDL fibroblasts contain lysosomes, which are large membrane-bound vesicles containing a homogenous matrix that is more electron dense than the surrounding cytoplasm.

The PDL fibroblasts have some unique properties such as, they exhibit osteoblastic properties like alkaline phosphatase activity 230, responsiveness to parathyroid hormone 231 and the production of bone sialoprotein in response to 1,25-dihydroxyvitamin D3 231. Also, these cells have been shown to possess proteins related to the osteoblastic activity, including, osteocalcin 232, osteopontin 233, periostin 234, osteonectin, runt-related transcription factor-2 (RUNX-2) and osterix 235. It has been shown that the PDL fibroblasts possess receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin (OPG). Both RANKL and OPG play a key role in the bone metabolism 236. They also express desmoplakins which have been considered to protect gap junctions in these cells against cell transformation caused by cell contraction during orthodontic tooth movement and periodontal repair 237. The PDL fibroblasts may look alike microscopically, but they have been shown to have different sub-populations. Whether or not these sub-populations have been derived from a single progenitor cell is still not clear.

These cells also have immunological properties. It has been demonstrated that PDL fibroblasts have functional characteristics of leukocytes and leukocyte-derived cells, functioning in innate immune response 238. Furthermore, it has been demonstrated that on stimulation with bacterial lipopolysaccharides, PDL fibroblasts up-regulate transcription of various cytokines and chemokines 238.

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Is PDL collagen degradation extracellular or intracellular:

The degradation of the PDL collagen fibers was historically considered as an extracellular process which involved collagenases. In extracellular collagen degradation, collagenases are responsible for cleaving the triple helical portion of the molecules within the fibrils into 1/4-3/4 fragments with further degradation of these molecules by gelatinases. Before initiation of the collagenase activity, the surface glycoproteins are removed by stromelysins.Although collagen degradation is an extra-cellular process, in PDL the collagen degradation is primarily an intracellular process. It has also been suggested that the intracellular collagen degradation is not unique to PDL but is found in all healthy tissues where there is controlled turnover and remodeling 239. Only in pathological tissue changes and/or when degradation is rapid and involves the whole tissue simultaneously, does the extracellular pathways have a role. 

Undifferentiated mesenchymal stem cells:

These cells are predominant in the central portion of the ligament, in close proximity to the blood vessels 240. These cells remain within the PDL throughout life and are responsible for tissue homeostasis 241. These cells help in maintaining the normal PDL space as they have the ability to differentiate into the formative as well as resorptive cells.

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Periodontal ligament stem cells and periodontal regeneration:

A stem cell is the one which has the capability of self-renewal and differentiation into various cell lineages. Originally, the human mesenchymal stem cells (MSCs) were isolated from aspirates of adult bone marrow 242.







All these findings regarding stem cells isolated from the PDL suggest that these cells are of prime importance during periodontal regeneration.

Epithelial cell rests:

The epithelial cell rests of Malassez were first described by Malassez in 1885 from the sections of human teeth.  These cells are commonly seen close to the cementum with their distribution varying according to the stage of tooth eruption and the age of the subject 252-259. The exact function of these cells is unclear, but they could be involved in the periodontal repair/regeneration. These cells may also have an important role in the maintenance of PDL and differentiation of cementoblasts 260.  Because these cells are never in contact with the bone and a thin buffer zone of fibrous connective tissue separates them from the bone, they may possibly act as ankylosis inhibitors 261. With age, the cellularity of these cells decreases 262. The epithelial cell rests show rapid proliferation when cultured in vitro. So, these cells have been implicated in the development of periodontal cysts 261, 263 and periodontal pocket formation 257. The epithelial cell rests also express ameloblastin which is a non-amelogenin enamel matrix protein that plays an important role in the differentiation of ameloblasts and induction of cementoblasts in association with amelogenin 264. However, the exact function of ameloblastin in these cells is not clear 265.

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Epithelial cell rests of Malassez and periodontal regeneration:

Regeneration of the lost periodontal tissue due to periodontal diseases is the ultimate goal of periodontal treatment. Regeneration involves the formation of new cementum, new bone and attachment of new PDL fibers to newly formed cementum and bone 266- 268.












The presence of these cells at the strategically important position in periodontal tissues, their ability to secrete matrix molecules conducive to cementum formation and the presence of the characteristic features of an actively synthesizing cell warrants investigation of the role of these cells in periodontal regeneration.



Osteoblasts within the PDL are found on the surface of the alveolar bone. Their appearance and structure is similar to the osteoblasts found in any other part of the body. Active osteoblasts have strongly basic cytoplasm with a prominent nucleus which lies towards the basal end of the cell and a pale juxtanuclear area indicates the site of the Golgi complex. An active osteoblast demonstrates all the features of actively synthesizing cells, such as prominent rough endoplasmic reticulum and numerous mitochondria. Active osteoblasts make a layer of cuboidal-shaped cells on the surface of the bone and are connected to each other via gap junctions and also via simplified desmosomes. They also contact to the osteocytes lying within lacunae in the adjacent bone via gap junctions, thus creating a well-organized system through the bone tissue.

The precursor cells for the osteoblasts are seen adjacent to the layer of active osteoblast in the vicinity of adjacent blood capillaries. These cells possess a reduced cytoplasm and few organelles. These cells differentiate to form a mature osteoblast. These cells migrate to the surface of the bone via the body of PDL. Usually, around 85-90% of the bone surface is covered by bone lining cells which are flattened with scanty cytoplasm. Only 10-15% of the bony surface is lined by osteoblasts. The osteoblast remains in an active functional state for up to 20 days.


These cells are responsible for the formation of cementum. These cells deposit the collagenous matrix of cementum which then mineralizes. They have a distinct layer on the root surface, but are less regularly arranged as compared to osteoblasts lining the bone surface. They show structural similarity to the PDL fibroblasts but can be distinguished from them by their presence near cementum and presence of less rough endoplasmic reticulum but more mitochondria than PDL fibroblasts. These cells possess numerous glycogen granules and significant quantities of both intermediate and actin filaments in their cytoplasm. Numerous gap junction and desmosomal junctions are seen on the cell membrane.


These are the bone resorption cells, which play a key role in bone remodeling. These are large multinucleated cells found within the resorption lacunae of the bone. They have a ruffled border adjacent to resorbing surface, enclosed by a smooth ‘clear’ zone. They have numerous mitochondria near the ruffled border, suggesting their high metabolic activity. These cells resorb the bone in two stages. Initially, there is the demineralization of minerals from the bone margin and then exposed organic matrix is degraded. In inactive osteoclasts, the ruffled border is absent. The multinucleated cells which are associated with the cementum and dentine resorption are referred to as cementoclasts and odontoclasts, respectively.

Defense cells:

The PDL contains defense cells, including macrophages, mast cells, and eosinophils. These cells are involved in the generation of the immune response during periodontal inflammation. These cells have been described in detail earlier in ‘cellular components of gingival connective tissue’.

Ground substance:

The ground substance of PDL is made up of high water content of up to 70%. It is primarily composed of two main components glycosaminoglycans/proteoglycans and glycoproteins. The ground substance of PDL is composed of various glycosaminoglycans such as hyaluronic acid, heparan sulfate, dermatan sulfate, chondroitin sulfate and proteoglycans of which dermatan sulfate is the principal one. Major glycoproteins present in the PDL ground substance are fibronectin and laminin. These are discussed in detail as follows,

Glycosaminoglycans and Proteoglycans in PDL ground substance:

Glycosaminoglycans and proteoglycans are the primary components of the ground substance of PDL connective tissue.


Glycosaminoglycans are long chains of repeated disaccharide units comprising of hexosamine and uronic acid. These molecules act as a binding material and due to their hydrophilic nature, they hold large amounts of water 279. Following are the major glycosaminoglycans in PDL ground substance,

Hyaluronic acid:

This is a high molecular weight glycosaminoglycan having widespread distribution in the connective tissue, especially in embryonic tissues and cartilage. It can bind to CD44 molecules through which it adheres to other matrix components. The primary function of this molecule is hydration of the ground substance, mediating interactions between cells and matrix and supporting vascular development.

Chondroitin sulfate:

It is a proteoglycan composed of disaccharide units of “O” sulfated N-acetyl  galactosamine  and  D-glucuronic  acid. Depending upon the site of sulphation, the molecule is termed as chondroitin-4-sulfate or chondroitin-6-sulfate. It functions as a solvent in the extracellular matrix and binds various connective tissue elements.

Dermatan sulfate:

This molecule is similar to chondroitin sulfate except that glucuronic acid is exchanged by L-iduronic acid. These molecules engage the collagen fibers in the connective tissue and are especially predominant in the epithelial-connective tissue interface.


As already discussed in ‘ground substance of gingiva’, structurally proteoglycans have a core protein bound to one or more glycosaminoglycan chains. Various proteoglycans found in PDL ground substance are decorin, biglycan, CD44, fibromodulin, lumican, perlecan, versican and periostin 280, 281.


The name decorin is based on the ability of this proteoglycan to bind to collagen that can be seen with an electron microscope as “decorations” on the collagen fibrils 282, 283. This proteoglycan was formerly known as PG-S2, dermatan sulfate PG-II and PG-40. This molecule has a single glycosaminoglycan attachment site on core protein. This proteoglycan has been demonstrated in association with collagen fibers and fibronectin 284.  Decorin and biglycan are the most homologous (~57% identical based on human amino acid sequences) of all the small leucine-rich proteoglycans. Both of these play an important role during wound healing. After the injury, decorin and biglycan must be reproduced if complete healing is to occur 285.  Studies on decorin-deficient animals have demonstrated an important role of decorin in collagen organization of the PDL 286.


Biglycan is a dermatan/ chondroitin sulfate proteoglycan which was formerly known as PG-I 287. It is widely distributed in the connective tissue including articular cartilages, intervertebral discs, skin, tendons, bones, and gingiva. It is found in association with the cell surface and pericellular matrix 288. Biglycan appears to play an important role in the mineralization process, although the precise nature of its role is still to be determined. Decorin and biglycan appear to have antagonistic roles in mineralization process. Decorin appears to have an inhibitory role during mineralization 289 whereas biglycan is one of the mineralization nucleator 290. Biglycan has also been suspected to be a receptor of amelogenin expression and enamel formation 291.


It is a chondroitin sulfate proteoglycan primarily found in loose connective tissue. It is a large molecule thought to be secreted by fibroblasts 284. The core protein of the molecules consists of an epidermal growth factor- like and lectin-like amino acid sequences, whereas the amino acid terminal has a hyaluronic acid-binding region. There are 14 glycosaminoglycan attachment sites in the core protein. Versican plays an important role in facilitating the binding of cell surface glycoproteins to the extracellular matrix 292. It has also been reported to play a role in fibroblast migration 293.

Fibromodulin and lumican:

These proteoglycans are rich in keratin sulfate and bind to collagen fibers present in the PDL. It has got structural similarities with both decorin and biglycan. Because it binds to the collagen fibers, it may modulate the collagen fiber formation. Studies using knockout mouse models have suggested that fibromodulin and lumican are involved in the supramolecular organization of PDL collagen 294.



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The CD44 was formerly known as lymphocyte homing receptor or Hermes antigen 298-300. It is a transmembrane glycoprotein with its cytoplasmic domain associated with actin microfilaments. It can bind fibronectin, laminin, and collagen and it may also be a receptor for hyaluronan 301.


These are protein molecules, covalently bound to carbohydrates. They have a widespread distribution in the connective tissue. Their main function is of binding the cells to the extracellular matrix elements. Major glycoproteins found in PDL ground substance are fibronectin, laminin, nidogen, vitronectin, tenascin and thrombospondin. Fibronectin and laminin have already been discussed in the section on ‘macromolecular components of gingival connective tissue’.


Nidogens are ubiquitous basement membrane glycoproteins. Nidogens are also known as Entactins. There are two types of Entactins expressed in vertebrates named entactin-1 (~150 kDa) and entactin-2 (~200 kDa) (or nidogen-1 and nidogen-2).  These molecules bind non-covalently to the laminin and acts as a bridge between laminin and collagen Type IV. The nidogen-laminin complex is essential for the integrity of the basement membrane.


Vitronectin is a 75-kDa glycoprotein which has a widespread distribution in the mesenchymal tissues. The major function of this molecule is to bind various connective tissue elements. It interacts with the extracellular matrix through its collagen and heparin binding domains, and with cells through its RGD integrin-binding sequence. Another important function of vitronectin is that it is conducive to osteoblast differentiation.


This glycoprotein is a large molecule with star-shaped structure. The tenascin glycoprotein family includes tenascin-C, tenascin-R, tenascin-W, tenascin-X, and tenascin-Y. They bind to fibronectin and to proteoglycans, particularly the cell surface proteoglycan, syndecan. In PDL, tenascin-C has been shown to have a localized distribution toward the attachment zone to the bone 302.


These are a family of structurally related multifunctional, multimodular, calcium-binding extracellular matrix glycoproteins encoded by separate genes. There are five members in thrombospondin family which have been divided into two groups where thrombospondin-1 and -2 belong to group-A and thrombospondin-3,-4 and -5 belong to group-B. Thrombospondins have binding properties and it binds to various extracellular matrix components such as integrins, fibronectin, collagen, and laminin. Also, thrombospondins bind to various cells and platelets.

Normal periodontal ligament Space:


Vascular supply of periodontal ligament:

The main blood supply of PDL in the p The PDL is particularly rich in its blood supply because it not only has high metabolism but also has peculiar mechanical and functional demands. When occlusal forces are subjected on the PDL, they are not only absorbed by the ligament fibers, but also by means of tissue fluid transfer within the PDL space, also referred to as ‘hydraulic pressure distribution’. The most important vessels in maxilla providing arterial supply to the PDL are anterior and posterior superior alveolar arteries, infraorbital artery, and the palatine artery. In the mandible, these arteries are the mandibular artery, sublingual artery, the mental artery and buccal and the facial artery. Around the PDL, there are primarily three sources of blood vessels (Figure 1.10). These are,

Figure 1.10 The blood supply of teeth and periodontal ligament

blood supply of periodontal ligament

Apical group of arteries: These are branches of vessels supplying the tooth pulp.

Alveolar group of arteries: These arteries enter the PDL space from the alveolar bone. These are also referred to as perforating arteries. They arborize in the coronal and apical direction.

Gingival group of arteries: These are derived from the gingival blood supply. These enter the PDL from the crestal region and anastomoses with the vascular network of PDL.

The venous and lymphatic vessels are located close to the blood vessels. The veins from the PDL drain either into the interdental veins or into the periapical plexus. The lymphatic vessels drain into the regional lymph nodes, finally draining into the thoracic duct.

Innervation of the periodontium:

PDL has both sensory and autonomic nerve supply. The sensory supply of PDL of maxillary and mandibular teeth is by the trigeminal nerve. In the maxilla, it is by the second branch and in the mandible, it is by the third branch of the trigeminal nerve. The sensory myelinated nerves enter the PDL at apical foramen region and run coronally, gradually losing their myelin sheath 307-309. Other nerve endings enter the PDL through alveolar bone and branch occluso-apically. In PDL “Ruffini-like” mechanoreceptor and nociceptive nerve fibers are present, which function to identify and transmit tactile stimulus as well as stimulus to stretching of the PLD fibers. The stimulus threshold of mechanoreceptors is lower as compared to pain-sensing nociceptive nerve endings. These two separate afferent systems are involved in providing us the information regarding the tooth movement, tooth contact during swallowing, chewing and the jaw position and pain under high occlusal load. This innervation system makes the teeth sensitive to identify even a hair between the occluding tooth surfaces.

The autonomic innervation originates from the superior cervical ganglion and is primarily responsible for the activation of the smooth muscles associated with vasculature within the PDL 310.

Functions of periodontal ligament:

The PDL performs four major functions: formative, proprioceptive, supportive and nutritive.

Formative function:

The development of PDL takes place from the cells of the dental follicle. Studies have shown that the transplanted cells of the dental follicle have the ability to form the PDL, alveolar bone and cementum 311, 312. This property of synthesizing three different tissues is retained in the PDL and it plays a critical role in periodontal repair and regeneration. Autoradiographic studies indicate a high turnover rate of the PDL collagen 182-185, 313, 314.

Nutritive function:

The blood vessels in PDL provide nutrition supply to the cells of PDL, cementocytes and presumably the superficial osteocytes of alveolar bone. The blood vessels are also responsible for the removal of catabolites. In trauma from occlusion, the excessive occlusal load results in the occlusion of the blood vessels leading to cell necrosis in the affected part of the PDL.

Proprioceptive function:

One important function of PDL is to provide sensory feedback during the masticatory cycle. As already stated, human teeth are capable of detecting very minute particles between the occluding surfaces. The sensory nerve endings in the PDL provide us the information about how hard and fast to bite. In a study, Williams et al. (1985) 315 anesthetized teeth and TMJs to measure differences in inter-incisor bite force. It was found that there was a significant discrimination of bite forces only when the teeth were anesthetized. These findings suggest that there is a well-established feedback mechanism in the PDL which plays a significant role in the proper mechanical function of the masticatory system by controlling the magnitude and duration of force application.

Supportive function:

Teeth are subjected to forces with different magnitude, direction of application and frequency of application during mastication, speech and orthodontic tooth movement. The PDL plays a central role in withstanding these forces and transferring them to the bone. It has been shown that because the forces during mastication are applied in different directions, both compression and tension areas exist in PDL during a regular loading scheme 306. The mechanical strength of PDL is derived from collagen Type I fibers 316. High degree of vascularization attributes to the viscoelastic behavior of PDL. The blood vessels present in PDL may contribute to “shock absorber” behavior of the PDL 317. It has been shown that the force applied and tooth displacement curve is non-linear for teeth. The initial resistance is low, but as the force is increased, the resistance increases and after it reaches higher levels the additional displacement is very small 318. Researchers have suggested a close fluid system in the PDL space which allows the distribution of large masticatory loads to the alveolar wall 318, 319. Another feature of PDL demonstrating its viscoelastic behavior is ‘hysteresis’. Hysteresis is the lag in the response of a material to the application or removal of a load. It is the property of a material to store energy and dissipate it slowly. Hysteresis in PDL is due to uncoiling and friction between principal fibers 320.

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The behavior of the periodontal ligament under forces:

As already stated, PDL plays an important role in transferring the occlusal forces from tooth to alveolar bone. Two theories have been explained for the mechanism of tooth support by periodontal ligament under occlusal forces,

Tensional theory: According to this theory, the principal fibers play a major role in supporting the tooth and transmitting the forces to the bone. On applying a load, principal fibers unfold and straighten to transmit the forces to alveolar bone, causing elastic deformation of the socket.

Viscoelastic theory:This theory emphasizes the primary role of fluid movement during tooth movement in the socket with fibers playing only a secondary role. On applying load on the tooth, the extracellular fluid is pushed from periodontal ligament into marrow spaces through the cribriform plate. When the load is removed, this fluid again returns back to PDL space and the normal fluid equilibrium is achieved.


Homeostatic function:

The cells of the PDL perform an important task of maintaining normal PDL space and neighboring structures. These cells are capable of resorbing and synthesizing the extracellular substance of PDL, cementum, and alveolar bone connective tissue. It must be remembered that these processes are continuous throughout life with varying intensity. The cells from PDL maintain the normal PDL space by directly influencing the bone deposition or bone resorption of the alveolar bone. This observation is supported by the finding that if a portion or the whole of PDL is irreversibly destroyed; bone deposition takes place in the PDL space resulting in ankylosis. Another finding associated with PDL homeostasis is the change in PDL space in hypo- and hyper-function. In teeth with hypofunction, the extracellular substance of PDL is lost, resulting in decreased PDL space. Conversely, during hyperfunction the PDL space is increased, presumably to compensate for the increased load.

Remodeling of periodontal ligament:

A well coordinated synchronized action of multiple cell types and signaling pathways is involved in the remodeling of PDL. The term remodeling and turnover should be differentiated here. Turnover constitutes no change in the structural organization of the tissue while remodeling implies positional or functional changes in the tissue. The remodeling of PDL is an important component of its property of adaptability to changes in the functional load 321. Primary cells involved in PDL remodeling are 123



Cementum is an avascular mineralized mesenchymal tissue covering the entire root surface. Although, it is an integral part of the tooth, but functionally it is a component of the periodontium. It was first described in 1835 329 and since then it has been studied extensively. It functions as the site of attachment for principal collagen fibers (Sharpey’s fibers) of PDL. Cementum has unique properties such as, it is avascular and lacks innervation, it does not express parathormone receptors (as do osteoblasts), so does not undergo remodeling as bone and its thickness goes on increasing throughout life 330, 331. The resorption of the cementum is less as compared to bone, so during orthodontic tooth movement, bone remodeling takes place with minimal effect on root cementum 332.

Development of cementum


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Classification of cementum

The cementum has been classified according to various factors, including presence or absence of cells, the nature, and origin of the organic matrix or combination of both.

Depending upon the presence or absence of cells:

  • Cellular cementum
  • Acellular cementum

Cementum has been traditionally classified into cellular and acellular, depending upon the presence or absence of cementocytes in its structure. The acellular cementum is the initially formed cementum found on the cervical portion of the root. Cellular cementum is found on the apical portion of the root and is deposited when the tooth enters its functional stage (Table 1.3). However, this arrangement is not always present and deviations do exist. Sometimes several alternate layers of these two variants are present, referred to as “mixed stratified cementum” (multiple interposed layers of acellular extrinsic fiber cementum and cellular intrinsic fiber cementum). The acellular cementum is generally formed before tooth eruption and prior to teeth reaching the functional occlusion. It is also known as primary cementum”. This cementum contains comparatively fewer collagen fibers which are placed more or less perpendicular to the dentinocemental junction. Subsequently, when teeth achieve occlusal contacts, cementum formed is known as the secondary cementum”. It is characterized by the presence of dense collagen matrix. It may be cellular or acellular 333.

Table 1.3

Differences between acellular and cellular cementum

Acellular cementum
Cellular cementum
Generally formed before tooth eruption and prior to teeth reaching the functional occlusionGenerally formed after tooth achieves occlusal contacts
It does not contain cellsIt contains lacunae and canaliculi containing cementocytes and their processes
Border with dentine not clearly demarcated Border with dentine clearly demarcated
Rate of development is relatively slowRate of development is relatively fast
Incremental lines are relatively close togetherIncremental lines relatively wide apart
Pre-cementum layer is narrowPre-cementum layer is wide
Usually more calcifiedUsually less calcified
Sharpey’s fibers are the main component and insert at right angle onto the root surfaceSharpey’s fibers occupy smaller proportion and are not the main component

Depending upon the nature and origin of the organic matrix:

  • Extrinsic fiber cementum
  • Intrinsic fiber cementum

There can be two sources of the organic matrix for the formation of cementum: fibers from the PDL or from the cementoblasts. When the fibers are derived from PDL, they are referred to as extrinsic fibers and when these fibers are derived from cementoblasts, these are referred to as intrinsic fibers. The extrinsic fibers or the Sharpey’s fibers are inserted into the cementum in the same direction as that of the principal fibers i.e. perpendicular or oblique to the root surface. The intrinsic fibers run parallel to the root surface and are oriented almost perpendicular to the extrinsic fibers. When both extrinsic and intrinsic fibers are present simultaneously, the cementum is then referred to as mixed fiber cementum.

Depending upon the time of formation, presence or absence of cells and on the nature and origin of the organic matrix:

This is the most commonly used classifications to describe various types of cementum. In this classification following types of cementum have been described,

  • Primary acellular intrinsic fiber cementum.
  • Primary acellular extrinsic fiber cementum.
  • Secondary cellular intrinsic fiber cementum
  • Secondary cellular mixed fiber cementum
  • Acellular afibrillar cementum

Primary acellular intrinsic fiber cementum:

This cementum is formed before the formation of the PDL, hence, the collagen fibers in its matrix are derived from the cementoblasts. When the thickness of this cementum reaches 15-20 μm, the fibrous fringes of this cementum come in contact with the PDL fiber bundles.

Primary acellular extrinsic fiber cementum:

This cementum is characterized by the presence of densely packed bundles of Sharpey’s fibers which are derived from PDL. It is usually found in the cervical third of the root, but may also be found further apically. Its thickness varies from 30-230 μm (Figure: 1.11). This cementum is acellular and does not contain cementocytes in its matrix. As its formation occurs after the formation of PDL, it becomes a principal attachment apparatus for PDL and cementum. This type of cementum is more mineralized than other types of cementum.

Figure 1.11 The ground section of tooth demonstrating acellular cementum

Ground section of tooth demonstrating acellular cementum

Secondary cellular intrinsic fiber cementum:

This cementum is formed of collagen fibers which are almost entirely derived from the cementoblasts. It must be noted here that the phenotype of cementoblasts which give rise to acellular cementum is different from those making cellular cementum. The later resemble that of the bone forming cells. This form of cementum is usually absent in incisor and canine teeth. It plays only a secondary part in the attachment of the cementum and PDL. This cementum is confined to the apical and the interradicular portion of the teeth. In humans, resorption lacunae are filled with this cementum. It may also contain the remnants of the Hertwig’s epithelial root sheath embedded in the calcified ground substance.

Secondary cellular mixed fiber cementum:

This cementum contains both Sharpey’s fibers derived from the PDL and fibers from the cementoblasts. This cementum forms the bulk of the secondary cementum. With light microscope, a lamellate structure can be seen in this cementum with the presence of cementoid on its surface. It is variably present on the root surface depending upon the functional state of the tooth. The cells in this type of cementum are placed haphazardly and depending upon the distance from the surface of cementum their viability differs. The cells, which are closer to the cementum surface get their nutrient supply from the PDL and are viable. As we go into the deeper layers, these cells loose intracellular organelles and ultimately die. Cementocytes possess cellular processes in the canaliculi but there is no evidence which suggests them forming a syncytium. The thickness of this cementum varies from 100-1000 μm (Figure 1.12a, 1.12b).

Figure 1,12a,b The ground section of the tooth demonstrating cellular cementum in (a) furcation area and (b) in apical area of the tooth

Cellular cementum in furcation area


Cellular cementum in apical area


Acellular afibrillar cementum:

As the name indicates, this type of cementum neither contains cells nor collagen fibers. It is a product of cementoblasts and is found only in the cervical areas of the tooth. The thickness of this cementum in humans varies from 1-15 μm. It plays no role in tooth attachment and is considered as a developmental anomaly.

Microscopic features of cementum

Microscopically, the acellular cementum appears relatively structureless. In the apical portion of the tooth, the most common presentation is that of cellular cementum covering the acellular cementum. However, variations can be seen. The difference between that rate of cementum formation in cellular and acellular cementum can be observed by the presence of a precementum layer and more widely spaced incremental lines in the cellular cementum. The cementocytes are observed inside spaces known as lacunae. In the ground section of the cementum, the cellular contents are lost and the empty spaces appear dark with air and debris filling them. The arrangement of cementocytes in the cementum is quite different from that of osteocytes in bone. As already stated the cementocytes are more widely dispersed and more randomly arranged with varying degree of spaces between them. The canaliculi of cementocytes are preferentially oriented towards the PDL, which is their primary source of nutrition (Figure 1.13).

Figure 1.13 The ground section of tooth under high magnification showing cementocytes

Ground section of the tooth showing cementocytes

Incremental lines are observed in cementum, which reflects the deposition of cementum in an irregular rhythm. These lines are the result of differences in the degree of mineralization. These lines are closer in acellular cementum as compared to cellular cementum.

Composition of cementum

123123 other calcified tissues such as bone, dentin, and enamel. The principal mineral component of cementum is hydroxyapatite [Ca10(PO4)6(OH)2] with small amounts of amorphous calcium phosphates. The transmission electron microscopic examination has demonstrated that hydroxyapatite crystals are found mainly between the collagen fibrils with their c-axis parallel to the long axis of collagen fibrils 335. The crystallinity of cementum is comparatively less as compared to other calcified tissue, because of which cementum is decalcified more easily. On the other hand, due to less crystallinity, cementum has a greater affinity for adsorption of environmental ions such as fluoride ions, as compared to other calcified tissues. This is the reason why in a mature tooth the fluoride ion concentration is highest in cementum as compared to other calcified tissues 350-352.

Know more…….Role of extracellular matrix (ECM) in periodontal regeneration:

The extracellular matrix makes the three-dimensional structure and acts as a foundation for the formation of mature tissue. It is primarily composed of collagenous and non-collagenous proteins. These components of ECM perform important roles during periodontal regeneration. These are as follows,

  • They act as a substrate for cell adhesion 353.
  • They facilitate cell migration thereby facilitating spreading of cells 353.
  • They determine and facilitate the development of a three-dimensional structure of matrix 354.
  • They regulate expression of growth factor and their receptors 355.
  • They also regulate the cellular response to growth factors 355.
  • They can influence the signaling pathways which are involved in biologic functions 355.


Cementum and enamel junction:

The thickness of cementum reduces in the coronal direction to end in the vicinity of the cervical region (Figure 1.14). The cementum and enamel relation is variable. In 60-65% of instances, cementum overlaps the cervical enamel. In around 30% of cases, the cementum touches but does not overlap the enamel. In 5-10% of instances, there remains a gap between the cementum and enamel, leaving exposed dentin In around 30% of cases, the cementum touches but does not overlap the enamel. In 5-10% of instances, there remains a gap between the cementum and enamel, leaving exposed dentin (Figure 1.15). All these relationships may exist on a single tooth.

Figure 1.14 Tooth section showing cementoenamel junction

Tooth section showing cementoenamel junction

Figure 1.15 The relation of enamel and cementum at cementoenamel junction

Relation of cementum and enamel at CEJ

Functions of cementum

There are three major functions of cementum. Firstly, it provides attachment to Sharpey’s fibers of the PDL, thus attaching the tooth to the alveolar bone. Secondly, it is involved in maintaining the normal PDL space. Finally, it serves as a medium through which the damage to the root surface is repaired.


It is an abnormality associated with the formation of excessively thick cementum on the root surfaces, which may affect an individual tooth or multiple teeth.  The generalized hypercementosis may be a hereditary condition and has been described in conjunction with Paget’s disease 356. The cementum thickening is more marked in the apical third of the tooth. In localized hypertrophy, spur or prong-like projections of cementum can be seen. These are usually seen in teeth subjected to greater stress. Teeth which are not in function have thickened cementum around the entire root surface with reduced number of Sharpey’s fibers.


These are small globular masses of acellular cementum found within the PDL. They are usually less than 0.5 mm in diameter. It has been proposed that they originate from foci of degenerating epithelial cell rests of Malassez in PDL 357. These may lie free in the PDL space (free cementicles) or may be attached (attached cementicles) to the radicular cementum. The attached cementicles eventually get incorporated into the cementum (interstitial cementicles). There is no significant clinical significance of the cementicles until they are exposed to the oral environment, where they may act as plaque accumulation factors.

Permeability of cementum

In health, cementum has a porous matrix because of which it is permeable to water and certain inorganic ions. However, on a diseased root surface, cementum is permeable to salivary organic components and plaque bacterial byproducts. It has been shown that on a plaque associated root surface, the bacterial products are present up to the depth of 10 to 12 μm 358. The bacterial lipopolysaccharides have been detected at a distance of 70 μm from the periodontally diseased root surface 359. Another factor associated with the permeability of cementum is bacterial penetration. Bacteria invading the cementum have been demonstrated in studies 358. It has been proposed that the bacteria penetrating the root cementum can act as a reservoir of periodontopathogenic bacteria 360. The permeability of cementum reduces with age 361.

Age changes in cementum

The cementum deposition occurs at a linear rate throughout life 362. Like bone, cementum is a dynamic tissue and it responds to the occlusal forces and orthodontic forces. The cementum is thickest in the apical areas of teeth and in furcation areas of multi-rooted teeth 363. It has been proposed that the thickness of cementum is increased by tensional forces 364. However, no clear-cut relationship between functional stress and cementum thickness has been demonstrated. The incremental lines in cementum demonstrate the changes in the rate of cementum deposition during different time periods. With increasing age, the thickness of cementum increases. It has been shown to triple in thickness between the ages of 20 and 60 years 365. This factor can be used in the determination of age in forensic dentistry. The thickness of cementum on the distal root surfaces is more than on the mesial root surfaces 366. Continuous cementum deposition is essential for the mesial drift of the teeth as well as the compensatory eruption of teeth accounting for the occlusal wear.

Changes in cementum associated with periodontal involvement

Many changes are observed in the cementum of a periodontally involved root surface. The main changes observed are breakdown of dentogingival fibers, loss of collagen fiber cross banding and dissolution of inorganic content of the cementum 367, 368. Areas of hypermineralization in cementum have been demonstrated by chemical 352, 369, microradiographic 368, 370-372, and SEM-microprobe 350 investigations.  However, some investigators did not observe any changes in the cementum mineralization on a diseased root surface 373, 374.  A detailed description of changes in cementum exposed to oral environment due to pocket formation has been given in “Periodontal pocket”.

Cementum resorption:

As already stated, PDL is the most important factor which prevents the root resorption. It has been proposed that cells derived from PDL are not only responsible for osteogenesis and osteoclasis, but also for fibrogenesis and fibroclasis in the ligament itself, as well as for cementogenesis and cementoclasis on the root surface 266.  Permanent teeth do not undergo physiological resorption as do the primary teeth. However, areas of cementum resorption at the microscopic level can be seen. In general, areas of cementum resorption increase with age. One study showed that 90.5% of teeth showed areas of cementum resorption in adult teeth 375. Bay like concavities can be seen under the microscope in the areas of cementum resorption. Adjacent to areas undergoing resorption, multinucleated giant cells, and mononuclear cell are generally seen.

Many factors such as inflammation, mechanical trauma, trauma from occlusion 376, orthodontic tooth movement 377-379, periapical pathology and pressure from the malaligned erupting tooth are associated with the resorption of cementum. Teeth without a functional antagonist and replanted/transplanted teeth 380, 381 may also show areas of cementum resorption. Systemic diseases associated with cementum resorption include hereditary fibrous osteodystrophy 382, Paget’s disease 383, hypothyroidism and calcium deficiency 384.

The repair of cementum occurs by deposition of new cementum, which can be easily identified by reversal lines. These deeply stained irregular lines delineate the areas of new cementum formation over pre-existing cementum. These lines are rich in proteoglycans and mucopolysaccharides with the presence of a few collagen fibers 385. The cementoblasts which deposit new cementum are derived from the surrounding connective tissue, most probably from PDL. However, the exact source of these cementoblasts and the molecular factors which regulate the cementoblast activity has still not been identified. Research has demonstrated that under specific conditions, the epithelial cell rests of Malassez may play an active role in cementum repair and regeneration 271.


Ankylosis is the result of abnormal repair where the PDL space is obliterated with the fusion of cementum and alveolar bone. Clinically, ankylosis is identified by a metallic sound on percussion. However, it must be noted that a definite diagnosis of ankylosis can only be made when at least 20% of the root surface is affected 386.  The radiographs demonstrate obliteration of the PDL space with the root and bone blending into a moth-eaten appearance. These teeth may remain functional for several years before they undergo resorption and finally exfoliation. The rate of resorption seems to be dependent upon the metabolism of the patient 387. Usually, ankylosed teeth loose their root within 4-5 years. In an ankylosed tooth, proprioception is lost because of the loss of PDL in the ankylosed area. The receptors for pressure are lost or they do not function correctly to sense the direction and magnitude of pressure. The ability of tooth to move is completely lost and the physiological mesial migration is stopped. In the dental implant treatment, the titanium implants are ankylosed with the bone. Because the titanium implant surface cannot be resorbed, they remain indefinitely ankylosed with the bone. This fact serves as the basis for dental implant treatment.

Know more……………Role of cementum in periodontal regeneration:

As already stated, cementum is anatomically a part of the tooth but functionally is considered as an integral part of the periodontium. It provides attachment to the principal fibers of PDL. Various characteristics of cementum suggest its vital role in periodontal regeneration.







 It has also been demonstrated that the growth factors within the matrix of cementum affect cells of the gingiva, PDL, and alveolar bone 395. All these findings suggest a significant role of cementum in the periodontal regeneration.

Alveolar bone


Alveolar bone is the specialized part of maxillary and the mandibular bone which supports the teeth. It forms with the eruption of teeth and gradually disappears after the tooth is lost. The alveolar bone consists of an outer cortical plate which is composed of Haversian bone and compacted bone lamellae, a central spongiosa or cancellous bone and inner socket wall. The cortical plate and the bone lining the socket wall (alveolus) meet at the alveolar crest. The bone lining the socket wall is referred to as “bundle bone” because it provides attachment to principal fiber bundles of PDL (Figure 1.16). Anatomically, alveolar bone is a quite complex tissue due to its functional demands. To understand various aspects of the alveolar bone structure and metabolism, we need to go through the developmental aspect and the molecular aspect of bone formation.

Figure 1.16 Cross section of the mandible at first molar region showing structural features of the alveolar bone

Alveolar bone

Basic concepts in osteogenesis

Bone is a dynamic biological tissue composed of metabolically active cells that are integrated into a rigid framework. The cell line involved in osteogenesis consists of preosteoblasts, osteoblasts, osteocytes and bone lining cells. These cells are of mesenchymal origin, derived from the stroma of bone marrow and from pericytes adjacent to small blood vessels in the connective tissue. Growth factors are involved in differentiation of these mesenchymal cells into osteogenic cells. These include various factors like transforming growth factor-β (TGF-β) and bone morphogenetic factor-2 (BMP-2) 396. Cell markers which indicate osteogenic differentiation are osteocalcin, osteonectin, alkaline phosphate and bone sialoprotein. The cells responsible for bone resorption are osteoclasts. Let us now try to understand how the bone forms.

Bone formation

Bone formation occurs by two mechanisms: intramembranous bone formation and endochondral bone formation. The intramembranous bone formation occurs by the inner periosteal osteogenic layer with bone synthesized initially without the mediation of a cartilage phase. On the other hand, endochondral bone formation occurs on a mineralized cartilage scaffold. The flat bones of the skull, maxilla and mandible are formed by intramembranous ossification. The main steps involved in intramembranous ossification are: formation of ossification center, calcification, formation of trabeculae and development of the periosteum. The mesenchymal stem cells are the primary cells involved in the initiation of bone formation. These cells differentiate into osteoblasts, which deposit osteoid at the site of bone formation.

During endochondral ossification, bone formation is initiated with the development of cartilaginous model followed by its growth. After this, the primary ossification center is formed where the process of ossification is initiated.  Then secondary ossification center/centers are formed which give rise to the final shape of the bone.

Know more……..Periosteum:

It is a well vascularized fibrous sheath which covers the external surface of most bones except the articular surfaces, areas of tendon insertions, or sesamoid bone surfaces. Periosteum contains osteogenic cells that regulate the outer shape of bone and work in co-ordination with inner cortical‘endosteum’ (tissue lining the internal bone cavities) to regulate cortical thickness and size. Periosteum consists of an outer fibrous layer and an inner cellular layer (cambium).The outer fibrous layer can be subdivided into two parts:







The cambium is thickest in the fetus and becomes progressively thinner with age. In adults, the cambium layer is so thin that it cannot be distinguished from the covering fibrous layer  400.

 Matrix orientation

Alveolar bone is basically composed of three types of bones: woven bone, cortical bone, and cancellous bone. The woven bone is immature bone, which is formed primarily during embryonic development, during fracture healing and in some pathological states such as hyperparathyroidism and Paget’s disease 401. The cortical bone (also known as compact or lamellar bone) is formed by the maturation of woven bone. It has a well organized vascular structure. The primary structural unit of cortical bone is an osteon. An osteon consists of a cylindrical-shaped lamellar bone that surrounds longitudinally oriented vascular channels known as ‘Haversian canals’ and horizontally oriented canals known asVolkmann canals’. The Volkmann canals connect the adjacent osteons. The third type of bone or the cancellous bone (also known as trabecular bone) has a honeycomb like structure with hematopoietic tissue filling the spaces within the bone. The trabeculae of the cancellous bone are mostly oriented perpendicular to external forces to provide structural support 402, 403.

Development of alveolar bone

As already stated, the alveolar processes of maxilla and mandible develop alongside with the eruption of teeth. During the second month of fetal life, there is the formation of a groove in maxilla and mandible that open towards the surface of the oral cavity, enclosing the developing tooth buds. Formation of alveolar bone starts with the formation of tooth supporting apparatus. A major portion of the alveolar process begins to form with root formation and eruption of the teeth.

The developing tooth buds in the maxilla and mandible are surrounded by loose woven bone spicules. With the development of the teeth, the trabeculae of the alveolar bone are formed. As permanent teeth develop, they start resorbing the roots of deciduous teeth which are ultimately shed. Finally, the permanent teeth occupy the alveolar sockets. The alveolar bone is formed around the teeth by intramembranous ossification.

Various parts of alveolar bone:

The alveolar bone is made up of two distinguishable parts, alveolar bone proper and supporting alveolar bone. The alveolar bone proper is made up of thin lamellae of bone (cortical bone) which surrounds the root. When seen on a radiograph, the alveolar bone proper appears as radiopaque line known as “lamina dura” (Figure 1.17). The principal collagen fibers (Sharpey’s fibers) from the PDL are inserted into this bone. Because of insertion of these fibers, alveolar bone proper is also known as “bundle bone”. The alveolar bone proper is perforated by many openings providing passage to the blood vessels, lymphatics, and nerves. Therefore, this bone is also known as “cribriform plate” (Figure 1.18).

Figure 1.17 Radiograph demonstrating radiopaque lining of the alveolar socket referred to as lamina dura

lamina dura

Figure 1.1 8 Alveolar bone housing of the tooth showing nutrient canals

Alveolar bone

The supporting alveolar bone is the remaining bone of alveolar process except alveolar bone proper. This bone consists of cortical bone and spongy bone. The cortical bone provides the outer covering to the alveolar process. It is lamellated and is covered by the periosteum. The inner and the outer cortical plates meet at the alveolar crest.  The thickness of the cortical plates in the posterior areas is usually about 1.5 to 3 mm. In anterior teeth, the thickness of cortical plates is highly variable. The cortical bone is thicker in the mandible than in the maxilla. The spongy bone is present between the outer and inner cortical plates. The trabeculae of spongy bone are arranged in two patterns,

Type I:  In this type, the trabeculae are arranged in a ladder-like fashion. This type of arrangement is more commonly seen in the mandible.

Type II: Here, the trabeculae are arranged in an irregular manner. These are more commonly seen in the maxilla.

Alveolar bone crest:

The alveolar bone crest more or less parallels the CEJ of the teeth, located 1-3 mm apical to it. This distance increases with age 404. The shape of the alveolar crest depends on many factors, including the contour of the CEJ, degree of tooth eruption and alignment of teeth. Similarly, the shape of the interdental bone crest depends on factors like the contour of the enamel, width of interdental space, the state of eruption and position of teeth in the arch. The contour of the alveolar bone margin is usually scalloped as described for gingiva, but it is not always the case. The contour of the crest of the bone margins depends on the shape of the roots and the thickness of the cortical plates. When the root is flat, the contour of the alveolar bone margin is also flat or straight. More curved is the root surface; more scalloped is the marginal bone. A thin bone covering the tooth roots is more scalloped as compared to thick bone which is more flattened.

The shape of interdental septum depends on the alignment of the cementoenamel junctions of the adjacent teeth and type of teeth. In anterior areas the interdental space is less, so the interdental septum is thin, whereas in posterior areas the interdental space is more so the interdental septum is thick. Thin interdental septa are also found in the posterior teeth where roots of the teeth are in close approximation. It is most commonly seen between the distobuccal root of the first molar and the mesiobuccal root of the second molar. An active periodontal disease results in a rapid bone loss in this area, ultimately resulting in tooth loss. Interdental and interradicular septa have canals known as canals of Zuckerkandl and Hirschfeld”. These canals house the interdental and interradicular arteries, veins, and nerves.

Dehiscence and fenestrations:

Dehiscence and fenestrations are commonly found in the alveolar bone. A dehiscence is the loss of alveolar bone on the facial (rarely lingual) aspect of a tooth that leaves a characteristic oval, root-exposed defect from the CEJ apically. A fenestration is a circumscribed hole in the cortical plate over the root surface which does not communicate with the crestal margin. In other words, we can say that unlike dehiscence, fenestration is bordered by alveolar bone along its coronal aspect (Figure 1.19) .

Figure 1.19 (a) Dehiscence (b) Fenestration





Composition of alveolar bone:

Like any other bone, alveolar bone is composed of around 65% of inorganic and 35% of organic proportions. Principal inorganic ions present in bone are calcium and phosphate. Other minerals present are carbonates, citrates and a trace amount of other ions including sodium, magnesium, and fluorine. The inorganic content is primarily made up of hydroxyapatite constituting around 65-70% of the bone structure.

More than 90% of the organic bone matrix is made up of collagenous proteins, primarily collagen Type I with a minor component of collagen Type V. The remaining portion of the bone matrix is formed of non-collagenous proteins, including hyaluronan, proteoglycans, GAGs (chondroitin sulfate, keratan sulfate) multi adhesive glycoproteins (osteonectin, sialoproteins I and II, Osteopontin), osteocalcin, growth factors and cytokines.

Cellular components of alveolar bone:


These are the bone forming cells, which express parathyroid hormone (PTH) receptors and have several important roles in bone remodeling including expression of osteoclastogenic factors, production of bone matrix proteins, and bone mineralization 405. Osteoblasts are derived from pluripotent mesenchymal stem cells and their differentiation is controlled by the master transcription factor RUNX2 (runt-related transcription factor 2); also known as CBFA1 (core-binding factor A1) 406, 407. During differentiation, osteoblasts express a specific cadherin referred to as OB-cadherin 408.

Osteoblasts secrete collagenous and non-collagenous matrix components of the bone matrix. They also secrete matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Many regulatory components such as cytokines and growth factors are also secreted by these cells. Because these are actively synthesizing cells, they contain abundant endoplasmic reticulum and Golgi complexes. During routine hematoxylin-eosin staining, these cells demonstrate intense basophilic cytoplasm. Mature osteoblasts, which are actively depositing bone matrix have a cuboidal or columnar shape.

Osteoblasts attach to the underlying bone via plasma membrane integrins, including α5β1, αvβ3, α3β1, α6β1 and α1β1 integrins located on the plasma membrane attachment plaques 409. These integrins bind to collagen and/or fibronectin in the bone, which is an essential step during bone formation. The expression of integrins on osteoblast cell membrane is downregulated by glucocorticoids. Recent research has revealed that osteoblast-lineage cells are involved in differentiation and activation of osteoclasts 410. Osteoblast lineage cells secrete macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor (NF)-kB ligand (RANKL) which are essential for osteoclastogenesis. RANKL is a member of the tumor necrosis factor (TNF) family. In addition, they also secrete osteoprotegerin (OPG), a decoy receptor for RANKL. Hence, the bone resorption by osteoclasts might be regulated by the balance of RANKL and OPG expressed in osteoblast-lineage cells. A detailed description of RANK, RANKL and OPG has been given in “Osteoimmunology in periodontal diseases”.


These are osteoblasts that get entrapped into the bone lacunae during bone deposition. These cells comprise more than 90% of bone cells within the matrix or on bone surfaces 411. They form a network of cytoplasmic processes extending through the cylindrical canaliculi to blood vessels and other osteocytes. The main function of these cells is, control of the extracellular concentration of calcium and phosphorus, as well as in adaptive remodeling behavior via cell-to-cell interactions in response to the local environment. Research has demonstrated that osteocytes can send signals of bone resorption to osteoclasts during bone remodeling 412. They are able to resorb bone on the lacunar walls and are also able to deposit new bone. The process of bone resorption by osteocytes is also known as “osteocytic osteolysis” 413.


These are the bone resorbing cells. Osteoclasts are multinucleated cells, which are controlled by various hormonal and cellular mechanisms. Macrophage-colony stimulating factor (M-CSF) is a critical factor for osteoclast differentiation along with a RANK / RANKL system which is responsible for osteoclast differentiation and maturation 414. Molecules like prostaglandin E2 (PGE2), interleukin (IL)-1, 1,25-(OH)2D3, parathyroid hormone (PTH) and PTH-related protein upregulate the expression of RANKL in osteoblast-lineage cells, thereby stimulating osteoclastogenesis. On the other hand, OPG, which works as a decoy receptor for RANKL inhibits osteoclastogenesis. Calcitonin, which is a hormone, also inactivates osteoclasts.

During osteoclast action, the plasma membrane in the area facing the bone matrix becomes folded (ruffled). This ruffled border is closely associated with bone resorption. Bone resorption is achieved by dissolution of mineral components consisting of hydroxyapatite and degradation of organic contents of bone matrix. The carbonic anhydrase (which converts CO2 and H2O into H+ and HCO3) and vacuolar-type H+-ATPase in ruffled border membrane result in the formation of shallow erosive pits on the bone surface called “Howship lacunae” 415. The chloride channel (CIC)-7 play an important role in the maintenance of cytoplasmic ion balance. The organic content of the bone matrix is degraded by lysosomal enzymes such as cathepsin K 416, 417 and MMP-9 418.

Know more………..The osteoblast and osteoclast coupling during bone remodeling:

There is a tight coupling of bone formative and resorptive activity during bone remodeling so that there is no net change in the bone mass and there is no qualitative change in the bone 419, 420.








These factors finally control the expression of osteoclast genes allowing the final differentiation of multinucleated osteoclasts.

Bone lining cells:

Bone lining cells cover inactive (non-remodeling) bone surfaces. These cells have a flattened shape and contain a few cell organelles. The intracellular characteristics of bone lining cells suggest that bone lining cells are hardly engaged in bone formation. Various terminologies have been used in the past to describe these cells, including surface osteocytes, inactive osteoblasts, endosteal lining cells and flattened mesenchymal cells. These cells are thought to be quiescent osteoblasts and are found in close proximity to each other, joined by adherens junctions. An extensive canalicular network connects the osteoblasts, osteocytes, and bone lining cells. The primary function of the osteocyte-osteoblast/lining cell syncytium is mechanosensation 424.

Functions of alveolar bone

The primary function of alveolar bone is to hold the teeth firmly in position and to transfer the occlusal forces to the basal bone. It is a dynamic tissue and adapts to withstand the occlusal forces put on the teeth. It provides vascular supply to PDL and cementum. It houses and protects the permanent teeth while supporting the deciduous teeth.

Remodeling and repair of alveolar bone

The alveolar bone is subjected to continuous remodeling to compensate for its functional demands. Initially, there is deposition of immature or woven bone. This bone is gradually replaced by mature or lamellar bone. The process of maturation is intimately related to the vascular bed. During lamellar bone formation, there is radial bone deposition around the central connective tissue core containing blood vessels and nerves. The density of bone minerals increases with time in an osteon to reach the peak level of mineralization.

Throughout the lifetime of an individual, there is a physiologic migration of teeth in the mesial direction towards the midline, also known as “physiologic mesial drift”.  To allow this mesial migration, the alveolar socket wall is resorbed on the mesial surfaces of the root and new bone is deposited on the distal surfaces of the socket wall. The bone resorption may be the result of mild PDL compression on the mesial root surfaces. On the other hand stretching of PDL on the distal surfaces of the roots may result in bone deposition. The PDL collagen fiber bundles get embedded into this new bone, which is referred to as “bundle bone”. The new bone is deposited on the older bone within a short duration of time. A “reversal line” separates the new bone from the older bone. The reversal lines usually have a scalloped outline that delineates the surface of last resorptive activity. The scalloped outline is formed due to resorptive bays created by osteoclasts during bone resorption.

The bone deposition or resorption also depends on the functional demand of the tooth. In tooth/teeth which are out of function, disuse atrophy of the alveolar bone results. Conversely, when the functional demand is increased, denser bone is formed. If the functional demand is more than the physiological tolerance of the bone, the bone density decreases.

Any fracture in the alveolar bone heals like any other bony fracture in the body. Within a few hours following fracture, the osteoprogenitor cells from the periosteum, endosteum and from bone marrow divide and migrate towards the site of injury. The blood clot which is formed between the fractured bone serves as a framework for cell migration and is rapidly populated by the immature osteogenic cells. The cells in the clot, including platelets and other cells derived from blood act as a source of various growth factors including bone morphogenetic proteins (BMPs), fibroblast growth factors (FGF), platelet-derived growth factor (PDGF) and insulin-like growth factors (IGFs), which are responsible for the stimulation of the cascade that leads to bone formation.  New blood vessels are formed which penetrate the clot within next 24 hours. Within a few days, callus is formed between the fractured fragments of the bone. Callus is composed of immature woven bone, which gradually remodeled to form mature bone.

Turnover of bone:

The turnover rate of alveolar bone is more than the other parts of the skeleton. The highest rate of remodeling is that of the cribriform plate, bone adjacent to PDL. The turnover rate of alveolar bone is particularly high during tooth eruption. During tooth eruption, there is rapid bone remodeling around the tooth till it reaches its final position in occlusion.


Periodontium supports the dentition and its components and allow interactions of teeth with occlusal forces and prevent their damage in function. The understanding of the structure and function of normal periodontium is essential to understand the changes that occur in periodontium in various pathological conditions. Each periodontal tissue is distinct in its location, tissue architecture, biochemical and cellular composition. In periodontal diseases, changes in the normal clinical features, histopathology, biochemistry of the tissues and their cellular composition are observed. The periodontal tissues have been thoroughly investigated for their structure at the molecular level, which has helped us to understand the biology of the periodontium in health and disease. This knowledge has been utilized to achieve regeneration of the lost periodontal structures in inflammatory periodontal diseases. We are still working on various aspects of periodontal regeneration and many aspects of periodontium still need to be investigated.

Periobasics: A textbook of Periodontics and Implantology
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References available in the hard copy of the website.

Periobasics: A textbook of periodontics and implantology

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