Periodontal pocket

The periodontal pocket is a pathological deepened gingival sulcus due to the apical migration of junctional epithelium. It may occur due to coronal movement of the gingival margin, apical displacement of epithelial attachment or a combination of the above. The coronal movement of the gingival margin (gingival enlargement) without destruction of underlying periodontal tissues is designated as a pseudo pocket, or gingival pocket, whereas apical migration of the junctional epithelium with the destruction of supporting periodontal tissues is designated as a true pocket or periodontal pocket.

Classification of periodontal pocket

The periodontal pockets can be classified on the basis of following criteria (Figure 22.1),

According to the relation between the base of the pocket and the crest of remaining alveolar bone:

  1. Suprabony (supracrestal or supraalveolar) pocket
  2. Infrabony (intrabony, subcrestal or intraalveolar) pocket

According to morphology:

  1. Gingival/false/relative pocket.
  2. Periodontal/absolute/true pocket.
  3. Combined pocket.

According to the number of surfaces involved:

  1. Simple pocket: It involves only one tooth surface.
  2. Compound pocket: It involves two or more tooth surfaces.
  3. Complex pocket: Where the base of the pocket is not in direct communication with the gingival margin. It is also known as a spiral pocket.

According to the nature of the soft tissue trail of the pocket:

  1. Edematous pocket.
  2. Fibrotic pocket.

According to the disease activity:

  1. Active pocket.
  2. Inactive pocket.


Figure 22.1 Classification of periodontal pockets

Classification of periodontal pocket

Table 22.1 differences between supra- and infrabony pocket

Suprabony pocket Infrabony pocket
The base of the pocket is coronal to the crest of the alveolar bone The base of the pocket is apical to the crest of the alveolar bone
The pattern of destruction of the underlying bone is horizontal The bone destructive pattern is vertical (angular)
Interproximally, the trans-septal fibers are arranged horizontally in the space between the base of the pocket and the alveolar bone Interproximally, the trans-septal fibers are oblique rather than horizontal. They extend from the cementum beneath the base of the pocket along the crest of interdental bone to the cementum of the adjacent tooth
On the facial and lingual surfaces, the periodontal ligament fibers beneath the pocket follow their normal horizontal-oblique course between the tooth and the bone. On the facial and lingual surfaces, the periodontal ligament fibers follow the angular pattern of the adjacent bone. They extend from the cementum beneath the base of the pocket along the bone and over the crest to join with the outer periosteum.

Formation of periodontal pocket depends on many factors which include the presence of local factors like plaque and calculus, anatomical position of the tooth, anatomical factors like lingual groove and host response. Initially, there is interplay of destructive and constructive tissue changes and the balance between them determines the progression of the disease process. Deeper pockets form over long periods of time due to continuous inflammatory reactions. Once a pocket develops, purulent exudates, food remnants, serum/blood by-products, dead bacteria, leukocytes and desquamated epithelial cells overlaying the layer of calculus or plaque are usually detected in the  periodontal pocket.

Pocket depth: It is the distance measured from the gingival margin to the base of the pocket. Pocket depth measurement is an essential part of the periodontal diagnosis.

Figure 22.2 Diagrammatic representation of healthy sulcus and different types of periodontal pockets

Periodontal pockets

Clinical attachment loss (loss of attachment): Under normal conditions, junctional epithelium is present at the cementoenamel junction. Any apical migration of this attachment is known as loss of attachment or clinical attachment loss. So, it is the distance from the cementoenamel junction to the base of the pocket or junctional epithelium. Clinical attachment loss can be in the form of a true pocket or recession or both of them (Figure 22.3). In the case of pseudopockets, there is no clinical attachment loss as the junctional epithelial attachment is at its normal position i.e. cementoenamel junction.

Figure 22.3 Clinical photograph of a patient having true periodontal pocket as well as recession

Periodontal pocket

Clinical features

The clinical features vary according to the severity of the condition. Usually, the gingiva appears bluish-red with thick rounded margins. On probing, there could be bleeding and suppurations. In deep chronic pockets, tooth mobility and formation of pathological diastema are evident. The patient may also report with sensitivity towards cold and hot, and an emergence of deep dull pain which could be localized or deep within the alveolar bone.

Mechanism of pocket formation

Our current understanding of periodontal pocket formation is the result of various studies done on ligature-induced lesions in animals 1-10, observations made from sections of the human maxilla and mandible 11-14, studies on neutropenic dogs 15 and broken mouth periodontitis studies done on sheep 16. Neutrophils play a very important role in the pathogenesis of periodontal pocket formation as they are the first line of defense around the teeth, epithelial barrier being the second 17. A detailed description of neutrophil function has been given in “Role of neutrophils in periodontal diseases”. As we know that bacteria are the primary etiology of periodontal diseases, the formation of periodontal pocket is the result of host-microbial interaction in the gingival sulcus. Following is the description of our current understanding of periodontal pocket formation,

  • Initially, there is plaque formation and accumulation of Gram +ve bacteria on the supragingival tooth surface. This plaque then extends into the subgingival
  • The process of periodontal pocket formation starts with plaque accumulation and its maturation. As the plaque matures, there is a microbial shift towards Gram -ve bacteria, which is the result of a change in subgingival environment. The ecological plaque hypothesis (P D Marsh, 2003) 18 explains the factors responsible for the growth of periodontal pathogens with changing subgingival environment, conducive for their growth.
  • The virulence factors produced by bacteria in the plaque stimulate the host immune response. These products are metabolic acids, bacterial lipopolysaccharides, FMLP (N- Formyl- Metheonyl-Leucyl-phenylalanine), volatile sulfur compounds, extracellular enzymes and fatty acids.
  • In response, the junctional epithelium cells produce various pro-inflammatory mediators like IL-8, TNF-α, PGE2, IL1-α and MMPs (Figure 22.4). Along with this, neuropeptides and histamine produced by free nerve endings causes vascular effects in that area. These mediators cause increased vascular permeability.

Figure 22.4 Mechanism of pocket formation

Periodontal pocket formation



  • The perivascular mast cells produce histamine, which causes the endothelium to release IL-8, which causes the polymorphonuclear cell recruitment. A large number of neutrophils transmigrate into the connective tissue under chemoattractant gradient produced by bacterial products and host immune cell products 19-21. These neutrophils rapidly pass through the junctional epithelial cells into the gingival sulcus. They form a variably thick layer over the subgingival plaque. Neutrophils covering the plaque surface are viable, but not completely functional 22, 23.
  • This layer of neutrophils prevents further extension and spread of bacteria by various antibacterial actions like phagocytosis. This action of neutrophils has been demonstrated by studies on neutropenic dogs. In normal dogs, even without tooth brushing the bacteria do not get access to connective tissue and pocket does not form, but in neutropenic dogs, regular tooth brushing also cannot prevent plaque extension subgingivally 15. Thus, proving important role of neutrophils in the defense against pocket
  • As the inflammation intensifies, there is degradation of connective tissue and gingival fibers. Studies have shown that just apical to junctional epithelium, there is degradation of collagen fibers and accumulation of inflammatory cells. The collagen fibers degrade by two methods, one by collagenases 24 and other enzymes of host and the bacterial origin and second by fibroblasts which phagocytize collagen fibers 25, 26. The junctional epithelial cells proliferate and form finger-like projections in the connective tissue.
  • There is an apical extension of junctional epithelium along the root surface. It is important to note that this process requires healthy epithelial cells. The degeneration of epithelial cells at the base of pocket actually retards pocket formation. The degenerative changes on the lateral wall of periodontal pocket are more severe than the base of the pocket.
  • The increasing number of transmigrating neutrophils interferes with the epithelial attachment and when the volume of neutrophils reaches approximately 60% or more of junctional epithelium, there is disruption of epithelial barrier creating an open communication between the pocket and the underlying tissue 27. This ulceration is the second important event in pocket formation.
  • Because of the disrupted epithelial barrier, the chemoattractant gradient is………..


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  • It is important to note that the healing process continues If the bacterial insult is stopped the junctional epithelium is again formed and destruction of connective tissue stops.
  • The transformation of the gingival sulcus into periodontal pocket results in the formation of the area where plaque removal becomes difficult, thus a feedback mechanism is formed as shown in Figure 22.5.


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Periodontal pocket and disease activity:

As discussed in the chapter 7 “Host-microbial interactions in periodontal diseases”, the periodontal disease process is not a continuous process, but consists of periods of quiescence and exacerbation. The clinical features of periodontal pocket are different in the quiescent period and active period of disease progression. During periods of quiescence, there is minimal loss of attachment and gingiva associated with periodontal pocket shows minimal signs of inflammation. During the period of exacerbation, which is initiated by plaque buildup, host-related factors and other factors; there is an accelerated attachment loss and deepening of the periodontal pocket. The gingiva associated with periodontal pocket demonstrates clinical signs of inflammation. There is bleeding on probing, which may be spontaneous or associated with probing and formation of greater amounts of exudate.  In the histological section, dense infiltration of polymorphonuclear cells 28 and plasma cells 25 can be seen. The epithelial lining is thin and areas of ulceration are evident in the pocket wall. A high proportion of motile organisms and spirochetes have been demonstrated during the active disease 29.

It must be remembered here that periodontal pocket depth is not an indicator of periodontal disease activity. The periodontal disease activity depends primarily on the phase of periodontal disease progression. During the active phase, there is accelerated periodontal destruction, whereas during quiescent phase there is minimal periodontal destruction. A shallow pocket during the active phase may demonstrate aggressive tissue destruction as compared to a deep pocket during a quiescent phase.


Histopathology of soft tissue wall of periodontal pocket

The cells of the epithelial attachment derive their nourishment from the lymph of the underlying connective tissue, but in a periodontal pocket, the chemical composition and hydrogen ion concentration of the underlying connective tissue is altered. Hence, the adjoining epithelial cells do not get their normal nutrition. As a result, those cells which are furthest from the source of nourishment, i.e. those in the superficial layers of the epithelial attachment that are nearest to the tooth, tend to undergo degenerative changes and split, thereby forming the first stage of pocket formation.

The principal periodontal fibers detach from the tooth and appear disorganized. Following the detachment of principal periodontal fibers, the epithelial attachment proliferates down onto the cementum of the tooth to occupy the area that was previously taken up by these fibers. The epithelium lining the periodontal pocket shows various degrees of proliferation and areas of small ulcerations are evident. There is proliferation of epithelial cells in the form of finger-like processes into ……….


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Studies have shown the presence of filaments, rods and coccoid organisms with predominant Gram-negative organisms in intercellular spaces of the epithelium 30, 31. Porphyromonas gingivalis and Prevotella intermedia have been found in the gingiva of aggressive periodontitis cases 32. Along with superficial layers, the bacteria can be found in the deeper layers of epithelial cell accumulating on the basement lamina.

Following the destruction of superficial fibers of the circular ligament, bone resorption is evident. Bone resorbing cells, osteoclasts can be seen at the bone crest, causing bone resorption. As the reparative process starts simultaneously, areas of bone apposition can also be seen.

Microtopography of periodontal pocket wall

Saglie et al. (1982) 33 investigated the soft tissue wall of periodontal pocket under scanning electron microscope. They observed different areas with different biological activity. The authors observed following areas starting from the superficial surface towards the connective tissue,

  1. Areas of relative quiescence (Demonstrating boundaries of the epithelial cells with occasional shedding of cells),
  2. Areas of bacterial accumulation (Demonstrating depressions on the epithelial surface, with abundant debris and a fibrin-like material. Bacterial plaque was seen penetrating into the enlarged intercellular spaces of the pocket epithelium),
  3. Areas of emergence of leukocytes (located in the periphery of the areas of leukocyte-bacterial interaction, where leukocytes appear in the pocket wall through intercellular spaces),
  4. Areas of leukocyte-bacteria interaction (area demarcated by numerous leukocytes emerging into the pocket wall, where they are frequently covered by bacteria in an apparent process of phagocytosis),
  5. Areas of epithelial desquamation (demonstrating areas of semi-loosened and folded epithelial squames with one end usually attached to the pocket wall surface and the other end free toward the pocket space),
  6. Areas of ulceration (areas with exposed connective tissue), and
  7. Areas of hemorrhage (with numerous erythrocytes).

Surface topography of tooth wall of periodontal pocket

The surface topography of the tooth wall of periodontal pocket has been studied by various authors 34-39. The following zones starting from the tooth surface outwards have been proposed based on these studies,

  1. Cementum covered by calculus: This zone consists of cementum, which has been covered by plaques and demonstrates various surface changes associated with dental plaque (discussed in the next section).
  2. Zone of attached plaque: In this zone plaque covers calculus and extends apically from it to a variable degree, probably 100 to 500 μm.
  3. Zone of unattached plaque: The zone of attached plaque is covered by unattached plaque, which extends apically to it.
  4. Zone where the junctional epithelium is attached to the tooth: This is the zone where the junctional epithelium is attached to the tooth. In a periodontal pocket, the extension of this zone is reduced to less than 100 μm as compared to the normal sulcui where it is usually more than 500 μm 40.
  5. Zone of connective tissue destruction: This zone lies apical to the junctional epithelium which demonstrates the connective tissue destruction.

Changes on cementum facing periodontal pocket

Presently, we are focusing on periodontal regeneration so in this respect changes on the cementum surface facing periodontal pocket play an important role. The deposition of plaque onto the root surface causes degradation of collagen fibers embedded in cementum. Pathologic granules can be found in areas of collagen degeneration 41. The acidic environment in this area may soften the cementum surface. Microorganisms in plaque get embedded into the cementum 42. Studies have shown bacteria in cementum, which can be found at cementodentinal junction 43, 44 and even in the dentinal tubules 45.

Areas of variable calcification can be found on the cemental surface. Hypercalcified areas can be found in areas where saliva is a constant source of minerals. The mineral content of exposed cementum is increased and chemical analysis shows an increase in calcium, magnesium, phosphorus and fluoride 46, 47. Hypocalcified areas can be found where ……………


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…………Whether cementum embedded with the bacterial endotoxins should be completely removed or only a smooth surface of cementum should be achieved is a matter of research, but from present data, it is clear that endotoxins cause structural changes in the cementum and may interfere with healing during periodontal treatment. However, a study done on beagle dogs demonstrated that healing was similar whether or not previously endotoxin exposed root cementum had been removed and that the removal of the root cementum for the purpose of eliminating endotoxins possibly present within the cementum is not necessary for accomplishing periodontal health 53. It has been demonstrated that extracts from diseased cementum are potent stimulators of monocyte secretion 54.

Our main aim of periodontal therapy is to produce smooth root surface, which provides a compatible surface for repair or regeneration. As regeneration is embedding of new periodontal ligament fibers into newly formed cementum, diseased cementum should be removed before we attempt regeneration. Root planning removes hypermineralized necrotic cementum, producing a smooth, sterile fresh surface for healing.

Other pocket associated facts

Site specificity:

The periodontal pocket formation is usually associated with few teeth in a dentition at a given point of time. On a particular tooth, the pocket formation may be only on a few sites around the tooth. Thus, periodontal destruction can be observed adjacent to a tooth with no periodontal breakdown. The severity of periodontal disease may increase, by the formation of periodontal pockets at new sites or by increasing of the periodontal pocket depth of existing pockets.

Periodontal pocket depth and loss of attachment:

It must be remembered that loss of attachment may or may not correlate with periodontal pocket depth. For example, two teeth having same pocket depth, one associated with the recession and the other with no recession have different loss of attachment. Tooth with the recession has more attachment loss. A shallow pocket may be associated with more attachment loss and a deep pocket may be associated with little bone loss. Furthermore, pockets with different depths may have a similar bone loss. Thus, the severity of bone loss must always be calculated by measuring the loss of attachment rather than pocket depth.

Pocket contents:

The periodontal pocket usually contains the following,

  • Debris consisting of microorganisms and their products
  • Gingival fluid.
  • Food remnants
  • Salivary mucin.
  • Desquamated epithelial Cells.
  • Plaque covered calculus.

In addition to the above contents, purulent exudate may be present in the pocket. It is mostly consisting of degenerated and necrotic leukocytes, dead bacteria, serum, and fibrin.

Significance of pus discharge from pocket:

It must be remembered that pus formation is a common finding in periodontal diseases, but it is only a secondary sign. Pus discharge from periodontal pocket does not indicate the severity of periodontal destruction. Furthermore, pus formation does not relate to the depth of the periodontal pocket. Shallow pockets may demonstrate extensive pus formation, whereas deep pockets may not. Thus, pus formation in periodontal pockets should be considered as the reflection of inflammatory changes occurring in the pocket and not as the indicator of disease severity.

Healing in a periodontal pocket

Periodontal pocket may be considered as a healing lesion. As stated above periodontal pocket formation has primary bacterial etiology. Breakdown of the periodontal tissue is accompanied by healing process that tries to compensate for the loss of periodontal connective tissue. Formation of new blood vessels is seen as an attempt to repair the damaged tissue. However, complete healing does not occur because of the constant presence of local irritants.

If the local irritants are not removed, the continuous healing process results in the fibrotic or edematous changes in the pocket wall. The fibrotic or edematous changes that take place during healing may not be considered as an indicator of changes occurring throughout the pocket wall, instead, they may be considered as the opposite extremes of the same pathologic process. The clinical features of the gingiva depend on the balance between pro and anti-inflammatory changes in the tissue. If the pro-inflammatory changes predominate, the pocket wall appears bluish-red, soft, spongy, and friable, with a smooth, shiny surface. If the reparative changes predominate, the pocket wall is more firm and pink. Clinically, the former condition is generally referred to as an edematous pocket wall and the latter as a fibrotic pocket wall.

If bacterial overload is reduced by doing non-surgical or surgical periodontal therapy, the healing process has an upper hand and healing takes place. But if the bacterial component is as such, complete healing never takes place because of the constant presence of irritants. So, the clinical features depend on the balance between the destructive and healing components.

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Periimplant tissue inflammatory response:

Similar to natural tooth the plaque accumulation around dental implants initiates an inflammatory response. However, this inflammatory response is not entirely similar in both the cases. To understand the difference in inflammatory response, one should know the differences between the connective tissue arrangement around the tooth and implant. The attachment of junctional epithelial cells around the tooth is facilitated by internal basal lamina and desmosomes along the entire length of the junctional epithelium. On the other hand, around dental implants, the attachment of the peri-implant epithelium to the implant surface is confined to the apical region only. Around tooth, the collagen fibers run in a perpendicular direction to be inserted on one side in cementum and on the other side into the alveolar bone. Whereas, around the implant, these fibers run almost parallel to the implant surface 55. However, fiber orientation in different directions has also been reported around the implants 56, 57. This difference in the soft tissue attachment around teeth and implants results in poor mechanical resistance of connective tissue attachment around implants as compared to the natural teeth 58. The connection between bone, periodontal ligament, and cementum around a tooth is resilient in nature, whereas there is a rigid connection around implants due to functional ankylosis/osseointegration and lack of periodontal ligament. The absence of the periodontal ligament leads to reduced tactile sensation and reflex function around the implants 59.

Due to these fundamental differences, the inflammatory response around the implant is different as compared to a natural tooth. More pronounced clinical and radiographic signs of destruction around the implants as compared to natural teeth have been observed in beagle dogs, where the periodontal and peri-implant lesion was induced by ligature-assisted subgingival plaque formation. Furthermore, the size of the soft-tissue lesion was found to be larger around the implants than teeth and it also extended into the bone marrow 60. Histomorphometric studies have revealed that the ratio of collagen, vessels, and plasma cells, around natural teeth and implants were comparable, but there were significantly lower proportion of lymphocytes, macrophages, and PMNs around implants. Hence, implants render a weak biological barrier to prevent the apical migration of inflammatory cells as compared to teeth 61. Furthermore, the extension of inflammatory cell infiltrate into the peri-implant mucosa was found to be more (~ 1.5 mm) as compared to the gingiva (~ 0.9 mm).



The periodontal pocket formation is the first step in periodontal breakdown cascade. Microbial etiology of periodontal pocket formation is well established. Present knowledge suggests that host-microbial interaction is involved in the initiation of the pocket formation. It must be understood that the above discussion is focused on general aspects of pocket formation. The periodontal breakdown is dependent upon the rate of disease progression, which varies among individuals. In the case of aggressive periodontitis, with minimal plaque deposits, we can see an aggressive periodontal breakdown. Various host and microbial factors are responsible for the disease progression, which includes virulence of the organisms involved, host immune response, environmental factors and genetic factors.


References available in the hard copy of the website

Periobasics: A textbook of periodontics and implantology

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