Analysis of Biomarkers and Marginal Bone Loss in Platform-Switched and Nonplatform-Switched Implants: A Randomized Clinical Trial.

Objectives: To compare the peri-implant crevicular fluid (PICF) biomarker levels, peri-implant status, and marginal bone level (MBL) differences of implants restored with randomly assigned nonplatform-switched (NPS) or platform-switched (PS) abutments. Methods: Ninety-four implants in 27 subjects were included in this study. Receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), interleukin-1ß (IL-1ß), monocyte chemotactic protein-1 (MCP-1) levels in PICF, peri-implant health, and the change in the MBL were evaluated at the time of restoration (T 1) and after 12 months (T 2). Results: The IL-1ß levels decreased and the RANKL, OPG, and MCP-1 levels increased from T 1 to T 2 (P < 0.05) in both groups. RANKL/OPG ratio at T 1, MCP-1 levels at T 2, and the MCP-1 change from T 1 to T 2 were lower in the PS group than in the NPS group (P < 0.05). MBL change was lower (0.51 ± 0.31 mm) in the PS group than that (0.75 ± 0.29 mm) in the NPS group at T 2 (P < 0.001). Peri-implant health status between the study groups was negligible. Conclusion: PS was superior to NPS regarding the preservation of MBL. Higher MCP-1 levels, altered RANKL/OPG ratio, and lower OPG levels in the NPS group could be associated with subclinical peri-implant bone remodeling.

An atypical form of necrotizing periodontitis.

BACKGROUND: Necrotizing ulcerative gingivitis/periodontitis are considered necrotizing periodontal diseases. This case report presents an atypical form of necrotizing periodontitis, which does not fit into this classification. METHODS: A 12-year-old child was referred to our clinic for gingival inflammation, extensive alveolar bone loss, and tooth mobility. Clinical and microbiologic examinations were carried out, and radiographs were taken. Clinical examination revealed soft and hard tissue destruction up to the mucogingival junction at the right maxillary premolar and mandibular incisors. Unusual infections or abnormalities in systemic functions were not detected through clinical and laboratory evaluations made at the Pediatrics Department, Istanbul University. Although an intensive established treatment protocol for necrotizing periodontitis was completed, management of long-standing health conditions could not be achieved because of recurrence of the disease, which caused us to repeat this treatment protocol at short intervals. RESULTS: Investigation led to a diagnosis of an atypical form of necrotizing periodontitis because the disease had a recurrent acute phase even under a standard treatment protocol. CONCLUSIONS: Our patient exhibits an unusual, necrotizing form of periodontal disease. The reason for the rapid rate of periodontal disease progression remains unclear.

Immunohistochemical analysis of the gingiva with periodontitis of type I plasminogen deficiency compared to gingiva with gingivitis and periodontitis and healthy gingiva.

OBJECTIVE: Type I plasminogen deficiency (Plgdef) is an uncommon chronic inflammation of mucous membranes. Gingival enlargements usually proceed with progressive periodontal destruction and tooth-loss. Plasmin(ogen)-independent enzymatic mechanisms for fibrin clearance have already been discussed in the literature. Our primary objective was to verify, immunohistochemically, the occurrence of different enzymatic factors involved in tissue breakdown of inflamed compared to healthy gingiva. Secondly, we tried to find out, if these patients have a similar microbiological profile to the patients with known gingivitis and periodontitis. MATERIALS AND METHODS: Immunohistochemical analysis of enzymes elastase, plasminogen (plg), cathepsin G, matrix-metalloproteinase (MMP)-3 and MMP-7 and of glycoprotein fibrinogen were performed with gingival tissues from 3 healthy controls, 8 patients with Plgdef and 3 patients with gingivitis and periodontitis. Furthermore, plaque from 5 patients with plasminogen deficiency were also obtained to determine the microbiological profile. RESULTS: Significantly high numbers of elastase positive leukocytes were detected in all samples. Staining for MMP-3 and MMP-7 was seen in samples with gingivitis and periodontitis with a stronger staining in samples with periodontitis by Plgdef. Fibrinogen was detectable in all samples. Staining for plg was stronger in samples with periodontitis than in other samples. Staining for cathepsin G was weak in gingivitis and periodontitis. Subgingival microbial flora showed elevated colony forming units of Prevotella intermedia/nigrescens, Fusobacterium spp., Eikenella corrodens, Porphyromonas gingivalis and viridans streptococci. CONCLUSION: Strong staining of elastase, MMP-3 and MMP-7 and weak staining of plg in Plgdef samples supports the plasmin(ogen) - independent fibrin clearance. Similar subgingival microbiological flora was observed in periodontitis with Plgdef as in other periodontal diseases. Further investigations should determine the exact pathomechanism and focus on effective treatment methods of this entity.