Clinical oral implants research · 2011
Reversibility of experimental peri-implant mucositis compared with experimental gingivitis in humans.
Контролируемое клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
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Salvi Giovanni E, Aglietta Marco, Eick Sigrun, Sculean Anton, Lang Niklaus P, Ramseier Christoph A
Аннотация
OBJECTIVE: To monitor clinical, microbiological and host-derived alterations occurring around teeth and titanium implants during the development of experimental gingivitis/mucositis and their respective healing sequence in humans.
MATERIAL AND METHODS: Fifteen subjects with healthy or treated periodontal conditions and restored with dental implants underwent an experimental 3-week period of undisturbed plaque accumulation in the mandible. Subsequently, a 3-week period with optimal plaque control was instituted. At Days 0, 7, 14, 21, 28, 35 and 42, the presence/absence of plaque deposits around teeth and implants was assessed, (plaque index [PlI]) and the gingival/mucosal conditions were evaluated (gingival index[GI]). Subgingival/submucosal plaque samples and gingival/mucosal crevicular fluid (CF) samples were collected from two pre-determined sites around each experimental unit. CF samples were analyzed for matrix-metalloproteinase-8 (MMP-8) and interleukin-1beta (IL-1β). Microbial samples were analyzed using DNA-DNA hybridization for 40 species.
RESULTS: During 3 weeks of plaque accumulation, the median PlI and GI increased significantly at implants and teeth. Implant sites yielded a greater increase in the median GI compared with tooth sites. Over the 6-week experimental period, the CF levels of MMP-8 were statistically significantly higher at implants compared with teeth (P<0.05). The CF IL-1β levels did not differ statistically significantly between teeth and implants (P>0.05). No differences in the total DNA counts between implant and tooth sites were found at any time points. No differences in the detection frequency were found for putative periodontal pathogens between implant and tooth sites.
CONCLUSION: Peri-implant soft tissues developed a stronger inflammatory response to experimental plaque accumulation when compared with that of their gingival counterparts. Experimental gingivitis and peri-implant mucositis were reversible at the biomarker level. Clinically, however, 3 weeks of resumed plaque control did not yield pre-experimental levels of gingival and peri-implant mucosal health indicating that longer healing periods are needed.
MATERIAL AND METHODS: Fifteen subjects with healthy or treated periodontal conditions and restored with dental implants underwent an experimental 3-week period of undisturbed plaque accumulation in the mandible. Subsequently, a 3-week period with optimal plaque control was instituted. At Days 0, 7, 14, 21, 28, 35 and 42, the presence/absence of plaque deposits around teeth and implants was assessed, (plaque index [PlI]) and the gingival/mucosal conditions were evaluated (gingival index[GI]). Subgingival/submucosal plaque samples and gingival/mucosal crevicular fluid (CF) samples were collected from two pre-determined sites around each experimental unit. CF samples were analyzed for matrix-metalloproteinase-8 (MMP-8) and interleukin-1beta (IL-1β). Microbial samples were analyzed using DNA-DNA hybridization for 40 species.
RESULTS: During 3 weeks of plaque accumulation, the median PlI and GI increased significantly at implants and teeth. Implant sites yielded a greater increase in the median GI compared with tooth sites. Over the 6-week experimental period, the CF levels of MMP-8 were statistically significantly higher at implants compared with teeth (P<0.05). The CF IL-1β levels did not differ statistically significantly between teeth and implants (P>0.05). No differences in the total DNA counts between implant and tooth sites were found at any time points. No differences in the detection frequency were found for putative periodontal pathogens between implant and tooth sites.
CONCLUSION: Peri-implant soft tissues developed a stronger inflammatory response to experimental plaque accumulation when compared with that of their gingival counterparts. Experimental gingivitis and peri-implant mucositis were reversible at the biomarker level. Clinically, however, 3 weeks of resumed plaque control did not yield pre-experimental levels of gingival and peri-implant mucosal health indicating that longer healing periods are needed.