Periodontal pocket


Periodontal pocket is a pathologically deepened gingival sulcus due to apical migration of junctional epithelium. It may occur due to coronal movement of the gingival margin, apical displacement of epithelial attachment or combination of above. The coronal movement of the gingival margin (gingival enlargement) without destruction of underlying periodontal tissues is designated as pseudo pocket or gingival pocket, whereas apical migration of the junctional epithelium with  destruction of supporting periodontal tissues is designated as true pocket or periodontal pocket. Before we discuss this topic in detail readers are advised to go through “The Immunology of Periodontal Diseases”.

Periodontal pocket

Periodontal pocket

Classification of periodontal pocket:

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

  1. Suprabony (supracrestal or supraalveolar) pocket
  2. Intrabony (infrabony, 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 surface 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 spiral pocket.

Depending upon the nature of the soft tissue trail of the pocket

  1. Edematous pocket.
  2. Fibrotic pocket.

Depending upon the disease activity

  1. Active pocket.
  2. Inactive pocket.

Differences between suprabony  and Infrabony pockets

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 transeptal fibers are arranged horizontally in the space between the base of the pocket and the alveolar bone Interproximally, the transeptal fibers are oblique rather than horizontal. They extend from the cementum beneath the base of the pocket along 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 upon many factors which include presence of local factors like plaque and calculus, anatomical position of tooth, anatomical factors like lingual groove and host response. Initially there is an interplay of destructive and constructive tissue changes and the balance between them determines the progression of disease process. The deep 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 over the layer of calculus or plaque can be visualized in a clinical examination.

Pocket depth: 

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

Clinical attachment loss (loss of attachment):

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

Clinical features:

The clinical features vary according to the severity of condition. Usually, the gingiva appears bluish red with thickened rounded margins. On probing there could be bleeding and suppurations. In deep chronic pockets, tooth mobility and formation of pathological diastma are evident. 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 periodontal 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 human maxilla and mandible11-14, 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 teeth, epithelial barrier being the second 17. For detailed description of neutrophil function please read “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 gingival sulcus. Following is the description of our current understanding of periodontal pocket formation,

Periodontal pocket formation

Periodontal pocket formation

  • Initially there is plaque formation and accumulation of gram +ve bacteria in the supragingival tooth surface. This plaque then extends to subgingival area.
  • The process of periodontal pocket formation stats with plaque accumulation and its maturation. As the plaque matures there is microbial shift towards gram –ve bacteria which is the result of change in subgingival environment. The ecological plaque hypothesis (P D Marsh) 18 explains the factors responsible for growth of periodontal pathogens with changing subgingival environment conducive for their growth. Read “Plaque as biofilm and the ecological plaque hypothesis” foe details.
  • The virulent 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 sulphur 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 MMP. Along with this neuropeptides and histamine produced by free nerve endings causes vascular effects in that area. These mediators cause increased vascular permeability.
  • The perivascular mast cells produce histamine which causes the endothelium to release IL-8 which causes the polymorphonuclear cell recruitment. Large number of neutrophils transmigrate into the connective tissue under chemoattractant gradient produced by bacterial products and host immune cell products 19-22. 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 23-24.
  • This layer of neutrophils prevents further extension and spread of bacteria by various anti-bacterial actions like phagocytosis. This action of neutrophils has been demonstrated by studies on neutropenic  dogs 25. In normal dogs even without tooth brushing the bacteria do not get access to connective tissue and pocket does not forms but in neutropenic dogs regular toothbrushing  also cannot prevent plaque extension subgingivally 26. Thus, proving important role of neutrophils in defense against pocket formation.
  • 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 27 and other enzymes of host and bacterial origin and second by fibroblasts which phagocytize collagen fibers 28-29 . The junctional epithelial cells proliferate and form finger like projections in the connective tissue.
  • There is apical extension of junctional epithelium along the root surface. It is important to note that this process requires healthy epithelial cells. That is why degeneration of epithelial cells at the base of pocket retards pocket formation. The degenerative changes on the lateral wall of periodontal pocket are more severe than base of pocket.
  • The increasing number of transmigrating neutrophils interferes with epithelial attachment and when the volume of neutrophils reaches approximately 60% or more of junctional epithelium there is disruption of epithelial barrier to create an open communication between the pocket and the underlying tissue 30. This ulceration is the second important event in pocket formation.
  • Because of disrupted epithelial barrier, the chemoattractant gradient is hampered. Because of this the neutrophils do not move in a particular direction and move randomly in the connective tissue. On the other hand the microorganisms get access to the connective tissue and this becomes a battlefield for host bacterial interaction.
  • Neutrophils perform their phagocytic function and release their granules because of which various enzymes accumulate in that area and execute their destructive functions.
  • Along with this activated macrophages produce various chemical mediators which further intensify the inflammatory reaction. These include IL-1β, IL-6, IL-10, IL-12, TNF-α, MMP, INF-γ and PGE2.
  • As the duration of the lesion prolongs, the antigen presenting cells activate the T-cell response which further activates B-cell response.  This host bacterial interaction continuous till there is bacterial infiltration. In due course of time the alveolar bone resorption starts which causes deepening of periodontal pocket. The pocket wall becomes densely infiltrated with plasma cells.
  • It is important to note that the healing process is continues throughout. If the bacterial insult is stopped the junctional epithelium is again formed and destruction of connective tissue stops. 

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 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 their source of nourishment, namely 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 tooth and appear disorganized. Following the detachment of principle periodontal fiber, 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 epithelial proliferation in the form of fingerlike processes into the underlying connective tissue. In the areas between the processes the epithelial layer is thin and an occasional microscopic breach may occur in its continuity thereby forming a microscopic ulcer. The superficial layers show signs of parakeratosis i.e. deficient keratinization. Most degenerative changes are seen on the lateral wall of periodontal pocket. The junctional epithelial attachment at the base of the pocket is much shorter (coronoapical length: 50-100 μm) than the normal sulcus.

These small ulcerations facilitates increased leucocytic infiltration from underlying connective tissue which is oedematous due to increased dilated and engorged blood vessels. It is densely infiltrated with plasma cells (approximately 80%), lymphocytes and PMN’sFollowing the destruction of superficial fibers of circular ligament bone resorption is evident. Bone resorbing cells osteoclasts can be seen at bone crest causing bone resorption. As the reparative process starts simultaneously, areas of bone apposition can also be seen.

It is important to note that the severity of condition does not depend upon depth of periodontal pocket. A relatively shallow pocket with ulceration may be more significant than a deep pocket with intact epithelium.

Studies have shown the presence of filaments, rods and coccoid organisms with predominant gram-negative organisms in intercellular spaces of the epithelium 31-32. Porphyromonas gingivalis and Prevotella intermedia have been found in the gingiva of aggressive periodontitis cases 33. Along with superficial layers the bacteria can be found in deeper layers of epithelial cell accumulating on the basement lamina.

Changes on cementum facing periodontal pocket:

Presently we are focusing on periodontal regeneration so in this respect changes on 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 34. The acidic environment in this area may soften the cementum surface. Micro-organisms in plaque get embedded into cementum 35. Studies have shown bacteria in cementum which can be found at cementodentinal junction 36-37 and even in the dentinal tubules 38.

Areas of variable calcification can be found on 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 increase in calcium, magnesium, phosphorus and fluoride 39-40. Hypocalcified areas can be found where plaque is constantly present. These are the areas where root caries is commonly found. The organism frequently associated with root caries is Actinomyces viscosus 41, but it may not be the only organism responsible for root caries 42. Along with this, other organisms associated with root caries are Actinomyces naeslundii, Streptococcus mutans, Streptococcus salivarius, Streptococcus sanguis and Bacillus cereus.

Endotoxins produced by plaque bacteria can be detected on root surface 43-44. Studies have shown that putting diseases roots in tissue culture induce irreversible morphologic changes in the cells of the culture 45. Whether cementum embedded with 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 cementum and may interfere in healing during periodontal treatment. A study done on beagle dogs demonstrated that healing was similar whether or not previously endotoxin exposed root cementum had been removed and the removal of the root cementum for the purpose of eliminating endotoxins possibly present within the cementum is not necessary for accomplishing periodontal health 46. It has been demonstrated that extracts from diseased cementum are potent stimulators of monocyte secretion, and that endotoxin as well as other factor(s) appear to be involved 47

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.

Healing in a periodontal pocket:

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


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 initiation of pocket formation. It must be understood that in the above discussion is focused on general aspects of pocket formation. Periodontal breakdown is dependent on rate of disease progression which varies among individuals. In case of aggressive periodontitis, with minimal plaque deposits we can see an aggressive periodontal breakdown. Various host and microbial factors are responsible for disease progression which include virulence of the organisms involved, host immune response, environmental factors and genetic factors. 


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Radius of action:

This term was first used by Grant and Cho. They pointed out that bone resorption stimulators produced by microbial plaque have a finite radius of action 48. Waerhaug investigated this principal on human periodontitis cases by doing histological sections, measurements on radiographs and extracted teeth to find out distance between microbial plaque and bone surface 49-52. His research has demonstrated that bone margin is never located closer than 0.5 mm to plaque and not farther than 1.5-2.5mm from plaque.

These findings indicate that when microbial plaque comes as close as 0.5mm of bone surface the bone resorption takes place. On the other hand the bone resorption stimulated directly or indirectly by microbial plaque is only effective for distance 1.5-2.5 mm. However, studies have shown that larger defects i.e. distance >2.5mm from plaque may be caused due to bacteria that are present in connective tissue 53-54.



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