Microbiological etiology of periodontal diseases is well established but present data strongly suggests equally important role of host immune response in pathogenesis of periodontal diseases. The initial response to bacterial infection is a local inflammatory reaction that activates the innate immune system causing release of an array of cytokines and other mediators and propagation of inflammation through the gingival tissues 1, 2. Due to initiation of bacterial and host immune interaction, destruction of periodontal connective tissue results which continues until the source of infection i.e. plaque is removed. Exaggerated immune response in some patient due to genetic factors can cause rapid breakdown of the tooth supporting structures. The details regarding the inflammatory response in gingivitis and periodontitis have been given in “Immunology of periodontal diseases” and “Periodontal pocket”. In the following sections we shall study the various aspect of periodontal bone loss.
Terminologies used to describe bony defects:
A periodontal defect surrounded by two or three bony walls or a combination of these.
A vertical defect that includes more than one surface of a tooth, e.g., a vertical defect that includes the mesial and lingual surfaces of a tooth.
It describes the depression in the bone crest between adjacent teeth, composed of buccal and lingual walls and two other walls created by the roots of the adjacent teeth.
Horizontal bone defect:
In this type of defect, bone loss is perpendicular to the long axis of the tooth, along the whole length of the alveolar bone crest, with occurrence of resorption of the buccal and lingual cortical plates, including the interdental bone.
Vertical bone defect:
It is located in the interdental bone and defined by oblique or angular orientation of the bone resorption in relation to the long axis of the tooth, with apical direction.
A vertical defect in the presence of adjacent roots; thus half of a septum remains on one tooth.
One wall, two wall and three wall defects:
Intrabony defects classified as one wall, two wall and three wall defects, depending upon walls remaining around the defect (described later).
Trench shaped defect:
A bony defect completely circumscribing the tooth like a trench.
Funnel shaped defect:
An intrabony resorptive lesion involving one or more surfaces of supporting bone; may appear moat-like.
Role of bacteria and inflammation in periodontal bone destruction:
Accumulation and maturation of plaque bacteria in gingival sulcus initiates an inflammatory response characterized by inﬁltration of leukocytes, which limit the level of bacterial invasion. The factors that regulate leukocyte infiltration include bacterial products, cytokines, cross-talk between innate and adaptive immune responses, chemokines, lipid mediators, and complement system. Following section describes the historical aspect of our understanding of etiopathogenesis of inflammatory periodontal diseases.
Initial studies identified a relationship between plaque accumulation and gingival inflammation. Löe et al. (1961)3 and Theilade et al. (1966)4, demonstrated a direct relationship between bacterial plaque accumulation and gingival disease. During same time period, animal experiments demonstrated a relationship among microbial plaque, inflammation, and periodontal bone loss 5-7. Other animal studies showed that treatment with antibiotics or topical application of chlorhexidine reduces the bacterial load and significantly reduces bone resorption 8, 9.
Then, with time different micro-organisms which cause periodontal bone resorption were identified. Animal experiments were done to verify pathogenicity of these micro-organisms. It was shown that introduction of Porphyromonas gingivalis into the oral cavity by oral gavage induced alveolar bone resorption in the mouse model 10-12. Similarly, Actinobacillus actinomycetemcomitans 13 and Tannerella forsythia 14 were shown to stimulate periodontal bone resorption.
The sustained microbial burden in periodontal arena is a source of continuous inflammation. Extension of this inflammation into deeper tissue causes bone resorption. The periodontal destruction occurs in an episodic, intermittent manner with periods of inactivity or quiescence. The exact reason for these active and in-active periods is not well established however, various theories have been put forward to explain this phenomenon:
Page and Schroeder (1982) 15 have associated the rapid bone loss during active periods to subgingival ulceration which elicits an acute inflammatory response.
Seymour et al.(1978) 16 have associated rapid bone loss with conversion of predominantly T-lymphocyte lesion into a predominantly B-lymphocyte lesion.
Saglie et al. (1987) 17 have postulated that connective tissue invasion by various bacterial species elicits an advanced host response leading to rapid bone resorption.
Newman et al. (1979) 18 have associated rapid bone loss with increased presence of loose, un-attached and motile gram –ve bacterial species in pocket anaerobic flora.
The extent, to which bacterial plaque can cause bone resorption, was also investigated. Page and Schroeder (1981) 19, showed that bone resorption form the site of bacterial plaque accumulation is upto 2.5-mm and beyond that it is caused by bacterial invasion of gingival connective tissue. These bacteria activate inflammatory response and hence, closer the cells of the inflammatory infiltrate to the bone, greater the number of osteoclasts formed resulting in greater amount of bone degraded 20, 21. In health, the amount of bone formation is equal to the amount of resorption that occurs and is referred to as coupling. This coupling is broken during inflammation resulting in net bone loss 22, 23.
With improvement in our understanding regarding host immune response, research work was focused on role of host response in periodontal destruction. Later on, role of cytokines and other chemical mediators was identified in bacteria-induced periodontal bone resorption. Presently, the role of cytokines like IL-1β, TNF-α and other chemical mediators is well established. A detailed description of molecular mechanisms involved in periodontal bone resorption in inflammation is given in “Osteoimmunology of periodontal diseases”.
Spread of inflammation into bone:
The spread of inflammation from gingival margin to underlying connective tissue and bone is responsible for bone resorption. The spread of inflammation occurs along the collagen fiber bundles and then following the course of blood vessels thorough loose connective tissue surrounding them into the alveolar bone 24. In inter-proximal areas, inflammation may spread directly from gingiva to the bone or from gingiva to periodontal ligament and then into bone or from gingiva to bone and then to periodontal ligament. Facially and lingually, inflammation spreads from gingiva along outer periosteum into the bone and into periodontal ligament.
Spread of inflammation from gingiva to supporting periodontal tissues
With the extension of inflammation into the underlying connective tissue, degradation of the gingival and trans-septal fibers takes place. These are broken down and their fragments can be seen in between the inflammatory infiltrate 25. Along with their destruction, repair also takes place to re-establish them. This is why; in advanced periodontal destruction these fibers can be seen.
As inflammation spreads into the bone marrow, it gets infiltrated by inflammatory cells such as leukocytes and mononuclear cells. The osteoclast differentiation is increased and the inner surface of bone lining is these cells. Subsequently, the fatty bone marrow is partially or completely replaced by fibrous bone marrow. The inflammatory process creates an environment for bone resorption, thus creating Howship lacunae. In persistent inflammation, loss of bone takes place thus reducing bone height in that area.
Kronfeld 26 in a classical study demonstrated that bone destruction taking place in periodontitis is not bone necrosis. The reason being, this whole process is being executed by living cells along viable bone. These findings were further supported by Orban 27. So, bone loss in periodontitis is not by necrosis of bone but by resorption of bone. The available bone is not infected or necrotic and should be preserved if possible.
Local factors determining patterns of bone resorption:
Teeth are surrounded by variable thickness of alveolar bone on different surfaces. In addition, the blood supply is variable in different parts of alveolar bone. For this reason pattern of bone resorption is random. Resorption follows the pathway of inflammation but that pathway may be different around different teeth. The pattern of bone resorption to a large extent depends upon mass of alveolar bone present in the region. Dehiscence is usually seen in areas with thin labial plate, where inflammation extends from marginal gingiva to apical direction.
In the same way if the investing bone is thick and marginal inflammation extends apically, the resultant pattern of bone resorption would be like trench or well. So, a funnel shaped defect results only when there is sufficiently thick mass of bone present and inflammatory process slowly cause bone resorption along the tooth; otherwise dehiscence will result.
Another major factor determining the bone resorption is anatomical location and tooth anatomy. Take an example of mandibular canine and lateral incisor. Because of its smaller dimensions, lateral incisor has a thick bone on the buccal aspect whereas canine has a thin bone. In addition to this, an insufficient contact relationship between these two teeth produces a conducive environment for pocket formation in this area. This causes formation of deep inter-dental craters.
In maxillary second molar, a flat shelf like bony excrescence extends from its mesial line angle to maxillary tuberosity. In mandibular molars, this type of bony architecture is provided by mylohyoid ridge on their lingual aspect. Both of these structures make these molars prone for formation of funnel shaped defects.
Presence of lingual tori and buccal exostosis:
Both lingual tori and buccal exostosis produce a similar situation as explained above in case of maxillary and mandibular molars. A thick bony mass present around teeth makes a conducive environment for pocket formation and later a funnel shaped defect.
A major requirement of crater formation is presence of thick mass of bone with guarding and thick buccal and lingual plates. This requirement is fulfilled by posterior teeth where the interproximal bone is sufficient to result in such kind of defect. Once the crest of the cortical plate is destroyed, formation of bony crater is quite rapid in these areas during chronic inflammation.
Presence of thick or thin periodontium:
The thickness of periodontium plays an important role in formation of osseous defects. A thin periodontium is commonly found around anterior teeth. Roots of teeth are embedded in relatively thin bone with a thin over laying soft tissue. This situation is not favourable for formation of craters, rather dehiscence and pyramidal bone loss are commonly found in this situation. After treatment usually these areas show gingival shrinkage and recession.
On the other hand thick periodontium presents an entirely different clinical situation. Here, the investing structures of the tooth are thick with thick alveolar housing around teeth. Inflammation of periodontium in these areas causes a circumferential bone loss around teeth which may vary according to the direction of spread of inflammation and other anatomical factors like root anatomy and tooth positioning.
Presence of trauma from occlusion (TFO):
Trauma from occlusion has been deﬁned as structural and functional changes in the periodontal tissues caused by excessive occlusal forces. Occlusal trauma is the overall process by which traumatic occlusion (occlusion that produces forces that cause injury) produces injury to the attachment apparatus. It may cause a thickening of the cervical margin of alveolar bone or a change in the morphology of the bone.
Irrespective of presence or absence of inflammation, trauma from occlusion causes bone destruction. In absence of inflammation TFO causes compression and tension on periodontal ligament. Excessive forces on periodontal ligament causes necrosis in affected areas and osteoclastic activity is also initiated causing bone resorption. Resorption of tooth structure can also result due to extension of osteoclastic activity. These changes are reversible and if offending forces are removed, repair of the injured tissues takes place. But, if the abnormal forces are not removed and tooth is under trauma for a long duration of time; a funnel shaped widening of the periodontal ligament can be seen in the crestal areas which later on causes bone resorption resulting in an angular bone defect.
Circumferential defect caused by trauma from occlusion
If TFO is associated with inflammation, the destructive effects of inflammation are enhanced. TFO modifies the spread of inflammation into the connective tissue thus resulting in aggravated tissue destruction. A complete description of trauma from occlusion has been given in “Trauma from occlusion”.
Role of systemic factors in bone destruction:
Systemic factors along with local factors play an important role in maintenance of normal bone physiology. Systemic factors may accelerate the rate of bone resorption by adding up into the local inflammatory component. Osteoporosis is a common condition in post-menopausal women which shares many common risk factors with periodontitis. Various studies have shown a relationship between skeletal bone density and oral bone density 28, 29. Various other systemic diseases such as hyperparathyroidism, leukaemia, Langerhan’s cell hystiocytosis etc. also cause bone loss but in a totally different way as compared to periodontitis.
Bone factor concept:
The bone factor concept was given by Irving Glickman 30. According to this concept there is a dynamic relationship between the local and systemic factors in maintenance of normal physiology of bone. If an individual has a generalized tendency for bone resorption, aggravated bone destruction can be seen in local inflammation. This concept helps us in determination of prognosis of an individual with periodontitis. For example, in post menopausal women the protective action of oestrogen on bone is downregulated because of its decreased levels. So, the bone factor and local inflammation in this case may cause more bone destruction as compared to a pre-menopausal women.
Classification of bone defects:
Goldman and Cohen (1958) 31, classified bony defects as suprabony, when the base of the pocket was present coronal to the alveolar crest and infrabony when the base of the pocket was present below the alveolar crest. Infrabony defects are of two types, intrabony defects and craters. Intrabony defects are bony defects whose infrabony component affects primarily one tooth, while in craters the defect affects two adjacent root surfaces to a similar extent. Infrabony defects have been classified according to their morphology in terms of residual bony walls, width of the defect (or radiographic angle), and in terms of their topographic extension around the tooth. According to the number of remaining walls, the intrabony defects have been classified as one wall, two wall or three wall defects. It is a broad classification of intrabony defects. Many times, more complex bone defects are encountered where a three wall defect in the apical portion becomes two or one wall defect in the coronal region. This is then referred to as combined osseous defect.
One wall defect
Two wall defect
Three wall defect
Clinical aspect of osseous defects and deformities:
In periodontal disease progression there are active periods of periodontal destruction which may be episodic or intermittent in fashion with periods of inactivity or quiescence. During active periods, signs of inflammation are evident with microscopically evidence of acute inflammatory reaction and ulcerations. There is loss of collagen and alveolar bone depending upon the disease activity. During inactive periods, signs of inflammation are minimal and reparative process is initiated. Bone formation can be seen immediately adjacent to the site of bone resorption and along trabecular surfaces at a distance from the inflammation. This bone formation is an effort to strengthen the remaining bone also known as “buttressing bone formation”. This repair causes formation of different bony deformities which can be seen clinically during surgical procedures.
Various bone destruction patterns in inflammatory periodontal disease:
Periodontal disease alters the morphologic features of the bone in addition to reducing bone height. An understanding of the nature and pathogenesis of these alterations is essential for effective diagnosis and treatment. Following patterns of bone loss are seen in periodontitis,
- Horizontal Bone Loss
- Vertical or Angular bone loss
- Furcation Involvements
- Osseous crater
- Bulbous Bone Contours
- Reversed Architecture
Horizontal Bone Loss:
Normally, the crestal bone is usually situated 1 to 2 mm apical to the cementoenamel junction. In periodontitis, due to bone loss the crestal bone is more than 2 mm apical to the cementoenamel junction. Bone loss is considered horizontal when the crest of the proximal bone remains parallel to an imaginary line drawn between the cementoenamel junctions of adjacent teeth. Horizontal bone loss may be localized or generalized. It is usually associated with suprabony pockets.
Vertical/angular bone loss:
Bone loss is considered vertical (angular) when the crest of the proximal bone is not parallel to the imaginary line drawn between the cemento-enamel junctions of adjacent teeth. Vertical bone loss is usually localized and related to such factors as trauma, calculus, subgingival plaque, overhanging restorations, and food impaction. It is associated with intrabony pocket formation. As already stated, vertical defects are broadly classified as one wall, two wall and three wall defects.
Vertical bone defects can be visualized in radiographs but in cases where thick buccal or lingual plates are present, it may be obscured. So, the most authentic way to correctly determine the bone defect is surgical exposure of the area. It has been shown that the frequency of occurrence of vertical bone defects increases with age 32, 33 and these are found more commonly on the distal surfaces 34 and mesial surfaces of the teeth 35, 36.
Vertical bone defect
Furcation involvement refers to commonly occurring conditions in which the bifurcations and trifurcations of multi-rooted teeth are invaded by the disease process. Furcation involvement is a stage of progressive periodontitis in which the apical extension of inflammation causes progressive attachment loss. The involved furcation may be visible clinically or it may be covered by the soft tissue. Other factors that may play a role are:
- Trauma from occlusion
- Presence of enamel projections
- Proximity of the furcation to the CEJ
- Presence of accessory pulpal canals in the furcation area
A detailed description of furcation involvement is available in “Furcation involvement and its treatment”.
Concavities in the crest of the interdental bone confined within the facial and lingual walls. These are one of the most commonly found bone defects which make around one third (35.2%) of all defects and about two thirds (62%) of all mandibular defects. There frequency of occurrence is twice in the posterior segment as compared to the anterior segment 37, 38.
Bulbous bone contours (exostosis):
These are bone enlargements caused by exostoses, adaptation to function or buttressing bone formation. These are found more frequently in maxilla than in mandible.
It is produced by loss of interdental bone, including the facial and lingual plates without loss of radicular bone.
It refers to a plateau-like bone margin caused by resorption of thickened bony plates.
The patho-physiology involved in patterns of bone destruction in periodontal diseases is a combination of destructive and reparative processes. The host response tries to repair the injury for re-establishment of normal structure and function of tissue. But, if the infection is persistent then these processes do not come to rest and various patterns of tissue response to injury can be observed.
The re-establishment of normal physiological bone contour is desired in surgical periodontal therapy. A detailed description of procedures involved in bone re-contouring and reshaping has been given in “Osseous resective surgeries”.
Classification of craters:
Craters were classified by Ochsenbein and Bohannan in 1964 39 as Class 1, Class 2, Class 3 and Class 4. Class 1 craters had 2-3 mm osseous concavity with relatively thick buccal and lingual walls. These were treated by palatal ramping. In class 2 craters the osseous concavity was 4-5 mm and thinner buccal and lingual walls. These were treated by buccal and palatal ramping. Class 3 defects had concavities of 6-7 mm with thin buccal and lingual walls and were treated by both buccal and palatal ramping. Class 4 were the lesions with variable depth and thin buccal and lingual walls.
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