Journal of periodontal research · 2013
Unexpected resilience to experimental gingivitis of subepithelial connective tissue grafts in gingival recession defects: a clinical-molecular evaluation.
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Graziano A, Cirillo N, Pallotti S, Cricenti L, Romano F, Aimetti M
Аннотация
BACKGROUND AND OBJECTIVE: The subepithelial connective tissue graft (SCTG) is the most widely used procedure for the treatment of gingival recession defects. Little is known, however, as to whether the apposed gingival flaps are more predisposed to develop plaque-related inflammation compared to healthy sites. This has salient clinical implications, as the long-term results of root coverage will depend largely on the level of inflammation of the grafted tissue.
METHODS: In the present split-mouth case-control study, clinical and biomolecular parameters were used to assess the level of inflammation of periodontal sites 12 mo after treatment with SCTG (test) and healthy non-treated gingivae (control) following the induction of plaque-related gingivitis in 19 patients.
RESULTS: The data showed that test sites had a significantly (P < 0.05) lower gingival index and angulated bleeding score compared to control sites (gingival index = 1.05 ± 0.23 vs. 1.34 ± 0.47; angulated bleeding score = 0.34 ± 0.37 vs. 0.61 ± 0.39) after induction of experimental gingivitis, whereas the plaque index did not differ in the two groups (P > 0.05). With regard to the biomolecular parameters, baseline levels of the proinflammatory cytokine interleukin-1β were higher in the gingival crevicular fluid of test sites. However, control sites exhibited more pronounced increase in the levels of interleukin-1β compared to test sites, upon plaque accumulation, so that the final concentration was similar in both groups. No changes were recorded in the gingival crevicular fluid volume.
CONCLUSION: Analysis of the data demonstrates that the sites of gingival recession treated with SCTG develop a lower degree of plaque-induced inflammation compared to healthy gingivae. This strongly suggests that SCTG does not predispose to inflammation and to further gingival recession and makes it a safe technique in the treatment of gingival defects.
METHODS: In the present split-mouth case-control study, clinical and biomolecular parameters were used to assess the level of inflammation of periodontal sites 12 mo after treatment with SCTG (test) and healthy non-treated gingivae (control) following the induction of plaque-related gingivitis in 19 patients.
RESULTS: The data showed that test sites had a significantly (P < 0.05) lower gingival index and angulated bleeding score compared to control sites (gingival index = 1.05 ± 0.23 vs. 1.34 ± 0.47; angulated bleeding score = 0.34 ± 0.37 vs. 0.61 ± 0.39) after induction of experimental gingivitis, whereas the plaque index did not differ in the two groups (P > 0.05). With regard to the biomolecular parameters, baseline levels of the proinflammatory cytokine interleukin-1β were higher in the gingival crevicular fluid of test sites. However, control sites exhibited more pronounced increase in the levels of interleukin-1β compared to test sites, upon plaque accumulation, so that the final concentration was similar in both groups. No changes were recorded in the gingival crevicular fluid volume.
CONCLUSION: Analysis of the data demonstrates that the sites of gingival recession treated with SCTG develop a lower degree of plaque-induced inflammation compared to healthy gingivae. This strongly suggests that SCTG does not predispose to inflammation and to further gingival recession and makes it a safe technique in the treatment of gingival defects.