Flap Debridement Essay

The periodontal tissue healing from flap debridement surgery is a repair process that wound after the event of healing does not have fully restored architecture or function. The most common periodontal tissue repair is by the formation of long junctional epithelium. This is supported by one of a couple classic studies by Stahl et al., which they observe healing response after open flap debridement with histologic evidence obtained 4 to 6 months after therapy. The histologic evaluation of the healing process showed the soft tissue adherence to the treated root surface, primarily an elongated junctional epithelium with connective tissue fiber oriented parallel to the root surface apical to the junction epithelium, resulting in pocket depth reduction.

The tissue apical to such soft tissue adherence was fibers functionally inserted onto the root which represented the zone undisturbed by the periodontal disease or the surgery.

Through histologic examination, there was no evidence of osteogenesis nor cementogenesis after flap debridement procedure, meaning that wound healing from such procedure is tissue repair rather than tissue regeneration. The clinical significance of such repair can be explained through the other study from the same group of researchers, by Froum et al., which also observed the healing response after open flap debridement with re-entries of the surgical sites after 6 to 7 months of healing. Clinical observation revealed a mean of 3.3mm of pocket depth reduction which consisted of an average of 1.4mm of clinical attachment level gain, and a mean 2mm of gingival recession, meaning the gingival margin had an apical shift after surgery. The osseous defect depth possessed a 2mm reduction, which is the combination of 1.2mm bone fill and 0.8mm of crestal bone resorption on average. The authors concluded that favorable healing response is positively correlated with frequent maintenance visits and proper plaque

control.

With clinical parameters improvement after open flap debridement and histologic evidence of wound repair by long junctional epithelium, to compare the resistance against bacterial plaque between long junctional epithelium and junctional epithelium of normal length, Magnusson et al., conducted an animal study on monkeys which they allow plaque accumulation around teeth previously ligated with elastic ligature and treated with flap surgery afterwards to allow long junctional epithelium formation, as well as periodontally healthy control teeth with normal intact dentogingival junction. Histologic results showed no difference in the inflammatory cell infiltrates induced by subgingival bacterial plaque between long junctional epithelium or normal intact junctional epithelium. Both groups exhibited inflammatory lesion in the connective tissue but did not have a deeper extension. The authors concluded that the barrier function against plaque infection of healed tissue is not inferior to normal periodontal tissue.