Within the limits of the present study, nicotine enhanced the effects of the local components of periodontal disease in a non-dose-dependent way; nevertheless, the administration of nicotine did not produce periodontal bone loss by itself.
The results show that the present microbiological and genetic parameters were not relevant for the prediction of periodontitis susceptibility in this family.
The present study investigated the effect of nicotine administration on periodontal breakdown resulting from ligature-induced periodontitis in rats. Twenty adult male Wistar rats were used. After anesthesia, a mandibular first molar was randomly assigned to receive a cotton ligature in the sulcular area while the contralateral tooth was left unligated. The animals were randomly assigned to one of the following treatments. of daily intraperitoneal injections: A - saline solution, B -0.37 mg of nicotine kg, C -0.57 mg of nicotine kg and D -0.73 mg of nicotine/kg. Thirty days later, the animals were sacrificed and the specimens routinely processed for serial decalcified sections. Statistical analysis (ANOVA) revealed greater bone loss (p<0.05) in the ligated teeth of animals which received nicotine (groups B/C D) than in the ligated teeth of animals which received saline solution (group A). In addition, a dose-dependent response was observed among the nicotine groups. A negative effect of nicotine was observed in the unligated teeth of the experimental groups (p<0.05). Therefore, daily administration of nicotine enhanced, in a dose-dependent manner, the effects of local factors in producing periodontal breakdown. Furthermore, the nicotine seemed to have a direct deleterious effect on the periodontal tissues.
We carried out a clinical evaluation of the hard tissue fill following treatment of ligature-induced peri-implantitis in dogs. Four dogs were used and their mandibular premolars (P2, P3 and P4) were removed. After 3 months of healing, two titanium implants were placed on each side of the mandible. After 3 months, the abutment connection was performed, and experimental peri-implantitis was induced by placement of cotton ligatures in a submarginal position. The ligatures and abutments were removed after one month, and the periimplant bone defects were assigned randomly to one of the treatments: debridement (control), debridement plus guided bone regeneration (GBR), debridement plus mineralized bone graft (BG), and debridement plus guided bone regeneration associated with a mineralized bone graft (GBR+BG). Clinical measurements of the peri-implant bone defects before and 5 months after treatment revealed no statistically significant differences between the defects treated by GBR, BG and GBR+BG. These 3 treatment methods provided more hard tissue fill than debridement alone (p < 0.05). Thus, it can be concluded that GBR, BG or a combination of the two techniques can enhance the hard tissue fill in defects caused by peri-implantitis in dogs. (
The purpose of this study was to evaluate, by histometric analysis, re-osseointegration following treatment of ligature-induced peri-implantitis in dogs. Five dogs were used in this study. Their mandibular premolars (P2, P3 and P4) were first removed. After 3 additional months of healing, two titanium implants were placed on each side of the mandible. After 3 months, the abutment connection was performed and experimental peri-implantitis was induced by placing cotton ligatures in a submarginal position. Ligatures and abutments were removed after one month and the peri-implant bone defects were randomly assigned to one of the treatments: debridement, debridement plus guided-bone regeneration, debridement plus mineralized-bone graft, and debridement plus guidedbone regeneration associated with mineralized-bone graft. Five months post-treatment, the degree of bone contact with the implant surface and the bone area within the threads were measured in 12 threads, the 6 most coronal at each side of each implant. One-way analysis of variance did not reveal statistically significant differences between the treatment modalities (p > 0.05). Within the limits of the present study, it can be concluded that there is a limited possibility of reosseointegration around implant surfaces previously exposed by ligature-induced peri-implantitis.
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