The purpose of this study was to perform a literature review of short implants in the posterior maxilla and to assess the influence of different factors on implant success rate. A comprehensive search was conducted to retrieve articles published from 2004 to 2015 using short dental implants with lengths less than 10 mm in the posterior maxilla with at least one year of follow-up. Twenty-four of 253 papers were selected, reviewed, and produced the following results. (1) The initial survival rate of short implants in the posterior maxilla was not related to implant width, surface, or design; however, the cumulative success rate of rough-surface short implants was higher than that of machined-surface implants especially in performance of edentulous dental implants of length <7 mm. (2) While bone augmentation can be used for rehabilitation of the atrophic posterior maxilla, short dental implants may be an alternative approach with fewer biological complications. (3) The increased crown-to-implant (C/I) ratio and occlusal table (OT) values in short dental implants with favorable occlusal loading do not seem to cause peri-implant bone loss. Higher C/I ratio does not produce any negative influence on implant success. (4) Some approaches that decrease the stress in posterior short implants use an implant designed to increase bone-implant contact surface area, providing the patient with a mutually protected or canine guidance occlusion and splinting implants together with no cantilever load. The survival rate of short implants in the posterior edentulous maxilla is high, and applying short implants under strict clinical protocols seems to be a safe and predictable technique.

ObjectivesChronic periodontitis is a common inflammatory disease of the oral cavity that causes destruction of periodontal tissues and bone around the teeth. Sclerostin is a protein encoded by the SOST gene. In this study, gingival crevicular fluid (GCF) levels of sclerostin in patients with chronic periodontitis were compared with those of healthy subjects.Materials and MethodsIn this case-control study, a total of 40 subjects were enrolled and divided into the healthy group (n=23) and chronic periodontitis group (n=17). GCF samples were collected, and the concentration of sclerostin was evaluated using enzyme-linked immunosorbent assay. Comparison of significance between groups was assessed using Mann-Whitney U test.ResultsSclerostin concentration was significantly higher in the chronic periodontitis group compared with the healthy group (P<0.005).ConclusionDespite the limitations of this study, sclerostin can be a possible marker for assessment of periodontal health status.

Nicotine has adverse cellular and molecular effects on oral mucosa, bone, and teeth. Vitamin E (α-tocopherol) and vitamin C (ascorbic acid) are biological antioxidants with positive effects on wound healing and bone formation. This in vitro study sought to assess the cytotoxic effects of different concentrations of nicotine and cotinine (a metabolite of nicotine) on MG-63 osteoblast-like cells and human gingival fibroblasts (HGFs) in the presence and absence of antioxidant vitamins E and C (separately and combined). Cell viability and proliferation were assessed using the methyl thiazol tetrazolium (MTT) assay. Cell migration was assessed using the scratch test, and expression of apoptosis-related genes was quantitatively analyzed using real-time PCR. Dose-dependent negative effects of nicotine on the morphology, viability, proliferation, and migration of MG-63 and HGF cells were statistically significantly greater than those of cotinine. Vitamin E (separately and combined with vitamin C) was statistically significantly more effective than vitamin C (at the concentration used in this study) at improving cell viability, proliferation, and migration, and at reducing apoptosis of cells exposed to nicotine or cotinine. Based on the positive results of this study, vitamin C and especially vitamin E (systemically and/or locally) may be useful in the repair and regeneration of oral hard and soft tissues in smokers.

Low concentrations of nicotine and cotinine caused a reduction in the initial cell adhesion. However, no significant adverse effects on the proliferation of attached cells were seen in the longer period. High concentrations of nicotine and cotinine have adverse effects on the cell adhesion and proliferation of HGF cells.

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