Abstract A reading of recent literature leads this reviewer to the conclusion that healing processes of treated periodontal lesions express variations of repair rather than regeneration. Specifically, the treated periodontal lesion repairs by 1) epithelial adhesion; at times occlusal to the base of the original pocket; 2) collagen adhesion; most frequently observed immediately apical to the newly adhering junctional epithelium but occlusal to the marginal alveolar crest, and 3) in the infrabony portion of periodontal lesions, simultaneous and/or sequential deposition of repair cementum, functionally oriented ligament fibers and narrowing of the vertical defect by osteogenesis. The supracrestal portion of such a periodontal lesion repairs as described above with new epithelial and collagen adhesions closing the gingival unit to the oral environment. The establishment of the supracrestal (trans-septal) fiber attachment may be the result of the remodelling of the vertical defect where repair cementum forms along the tooth wall of the vertical defect and acts as an anchor for fiber insertion. With the resorption of the crestal margin, repair cementum and inserted fibers are present on the root surface occlusal to the alveolar crest and may well serve as the new anchoring site for supracrestal fibers. Another possibility is the occlusal spill of connective tissue primarily from the periodontal ligament which includes supracrestal cementogenesis, thereby creating an environment for the insertion of new supracrestal fibers as part of flap healing. While the exact sequence of supracrestal fiber formation after treatment of vertical defects is not known, it should be emphasized that all specimens studied have shown their presence as part of a successful “fill”. Obviously, these repair sequences do not occur after every therapeutic intervention. However, sufficient documentation is available to acknowledge their possibility following various treatment modalities.
The description of the reviewed repair processes takes us a long step forward from the rather limited repair projected by Orban in 1948. Yet, it does not provide us with information regarding the viability of these repair tissues when confronted with continuing assault by plaque or other irritants. Do such tissues resist local injury as well as the normal attachment? Is the loss of adhesion following insult accomplished more quickly because the length of adhering tissues is significantly increased in an occlusoapical direction? Do host factors affect the repair tissues differently than normal tissues? The answers to these questions need extensive exploration regarding the nature of the repair tissues. But the recognition of the process has profoundly influenced clinical therapy and raised new questions regarding the factors controlling repair and possibly even regeneration following periodontal therapy.
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