Introduction to the periodontal pocket
The formation of a true periodontal pocket is the hallmark of periodontitis. It is characterized by the apical migration of the junctional epithelium from its normal position at the cementoenamel junction. Various investigators throughout history have tried to understand the exact mechanism of pocket formation. Historically, various theories of pocket formation have been proposed to explain the mechanism of pocket formation. Presently, the mechanism of pocket formation (as explained in “Periodontal pocket”) is well defined, however, for more information on pocket formation; we should also know what all mechanisms of pocket formation have been explained historically. These theories have been explained by various researchers as described below,
Skillen (1922) 62:
According to Skillen, the epithelial attachment offers a weak barrier for the spread of infection downwards in the connective tissue. When subjected to infection and/or trauma, pathological dissolution of the epithelial attachment takes place. This allows the apical migration of the epithelial cells and thus, pockets formation.
Gottlieb (1926, 1927) 63, 64
Gottlieb proposed that root surface changes are the main cause of pocket formation rather than the changes in gingival tissue. He stated that the down growth of epithelial attachment is a physiological process. However, because of the continuous passive eruption of the tooth and continuous deposition of new cementum, the apical migration of epithelium cannot occur at pathological rate. The newly deposited healthy cementum acts as a barrier for the apical migration of the epithelium. The inflammatory process is harmful to both cementum and gingival tissue and it also dissolved the organic union between the two tissues. Hence, because of the loss of this organic union, the epithelium migrates apically until it reaches the unaltered cementum and connective tissue fibers.
James and Counsell (1927) 65:
This theory proposes pocket formation in two stages. In the first stage, there is proliferation of the epithelial attachment. In the second stage, due to the loss of superficial layers of the epithelium, space is created which gives rise to the periodontal pocket. Because the rate of proliferation of the epithelium at sulcus base is such that it precedes the degeneration of epithelial cells in superficial layers, the pocket is always lined by the epithelium.
Beck (1929) 66:
This theory proposes that there is well-established coordination between degeneration of the enamel epithelium, proliferation f the oral epithelium and atrophy of the gingival papilla, which maintains the normal sulcus depth around 1 mm. Any disturbance in this coordination either by inflammation or trauma results in pathologic pocket formation. According to the Beck, pocket formation occurs between the oral epithelium and enamel epithelium rather than separation of enamel epithelium from the cuticle. If there is a ……….. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book..
Wilkinson (1935) 67:
According to this theory, pocket formation is the result of proliferation and down growth of epithelial attachment or oral epithelium with inflammation playing only the secondary role. The cause for the epithelial proliferation was unknown but the author considered vitamin A deficiency as its main cause. The epithelial proliferation results in thickening of the epithelial lining of the sulcus. Because of this thickening, the cells on the inner aspect of the sulcus get deprived of nutrition and undergo degeneration and necrosis. The degenerated epithelial cells become calcified and their separation from adjacent normal epithelium produces a pocket or trough. These changes result in the proliferation of the epithelium along the cementum and detachment of epithelium from its coronal portion from the root surface, thus resulting in pocket formation.
Box (1941) 68:
According to Box, periodontal pocket formation is either the result of imperfect junction between the epithelium and the cementum or too thin epithelial lining. Because of the bacterial invasion at the base of the sulcus, inflammatory changes occur that result in progressive destruction of the connective tissue. These changes and infective agents possibly related to Leptothrix falciformis are capable of periodontal pocket deepening.
Fish (1948) 69:
This theory proposed that the apical migration of the epithelial attachment is the result of the destruction of underlying gingival fibers. These fibers have proposed to act as a natural barrier for the apical migration of the epithelium. Due to the action of bacterial enzymes such as hyaluronidases, the fibers immediately adjacent to the epithelium are destroyed resulting proliferation of the epithelium downwards until the healthy fibers are reached.
Aisenberg et al. (1948) 70:
According to this theory, destruction of collagen fibers is not a prerequisite for the apical migration of the epithelial attachment. The inflammation caused by the bacteria and their products stimulates the apical migration of the epithelial attachment without preceding destruction of gingival fibers. The authors stated that the epithelium burrows between the intact gingival fibers and attach themselves further apically on bundle free areas on the cementum. The degradation of the fiber bundles is secondary to epithelial migration. The migrated epithelial cells enmesh the fiber bundles and degrade them slowly.
Nuckolls et al. (1950) 71:
This theory proposes inflammation as the primary cause of pocket formation. The inflammatory changes in the connective tissue instigate increased mitotic activity in the basal epithelial cell layer (sometimes in prickle cell layer) and increased keratin production with desquamation. The cellular desquamation adjacent to the tooth surface results in the initiation of pocket formation. According to the authors, ……… Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book..
A lot of research has been done to find out the exact mechanism of pocket formation. Although, the above stated theories are of historic interest; however, their knowledge is essential to understand the development of periodontal pocket in perspective. The immunulogical mechanisms involved in the pocket formation have been explained in “Host-microbial interactions in periodontal diseases”.