Periodontitis is an infectious inflammatory disease that results in attachment loss and bone loss. Regeneration of the periodontal tissues entails de novo formation of cementum, periodontal ligament, and alveolar bone. Several different approaches are currently being explored to achieve complete, reliable, and reproducible regeneration of periodontal tissues. The therapeutic management of new bone formation is one of the key issues in successful periodontal regeneration. Bone morphogenetic proteins form a unique group of proteins within the transforming growth factor superfamily of genes and have a vital role in the regulation in the bone induction and maintenance. The activity of bone morphogenetic proteins was first identified in the 1960s, but the proteins responsible for bone induction were unknown until the purification and cloning of human bone morphogenetic proteins in the 1980s, because of their osteoinductive potential. Bone morphogenetic proteins have gained a lot of interest as therapeutic agents for treating periodontal defects. A systematic search for data related to the use of bone morphogenetic proteins for the regeneration of periodontal defects was performed to recognize studies on animals and human (PUBMED, MEDLINE, COCHRANE, and Google search). All the studies included showed noticeable regeneration of periodontal tissues with the use of BMP.

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Background:Pathogenesis of most of the inflammatory process are associated with reactive oxygen species (ROS), derived from various metabolic sources and which may lead to direct or indirect tissue damage due to oxidative stress, resulting in periodontal diseases. Usually antioxidant systems are capable of removing free radicals, thereby preventing tissue damage from free radical. ROS can result in tissue damage, involving lipid peroxidation. The aim of this study was to evaluate and compare the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA), and sialic acid (SA) in periodontally healthy and chronic periodontitis among nonsmokers and smokers and to determine their value as diagnostic markers for chronic periodontitis.Materials and Methods:A total of 90 male patients aged 20--60 years were recruited and grouped as Group 1: 30 Healthy nonsmokers, who had never smoked. Group 2: 30 nonsmokers with chronic periodontitis. Group 3: 30 smokers with chronic periodontitis. Unstimulated saliva was collected for at least 5 min and clinical measurements; SOD, GPx, MDA and SA were assessed using a spectrophotometric method.Results:Data showed a significant correlation between salivary SOD, GPx, MDA, and SA in group 1, group 2, and group 3. SOD and GPx were found to be lower and MDA and SA levels were found to be higher among smokers with chronic periodontitis.Conclusion:Reduced levels of antioxidant enzymes SOD and GPx and elevated levels of lipid peroxidation product MDA as well as increased levels of SA could be used as diagnostic markers to measure oxidative stress in periodontal disease associated with risk factor such as smoking.

The study results suggested that among the patients with periodontal disease, serum VB12 levels are directly related while serum FA levels are inversely related to inflammation and tissue destruction in periodontium as occurred in Group IV.

Study background: Fluorosis is one of the manifestations of chronic poisoning from long-term exposure to high levels of fluoride. An estimated 62 million people in 17 states in India are affected with dental and skeletal fluorosis. Objective: To evaluate the cytological morphology of exfoliated oral mucosal cells among various stages of fluorosis patients compared with controls. Design and methods: Exfoliative cytology PAP-stained smears of 21 cases of fluorosis and 21 controls subjected to morphometric analysis using image Proplus software. For the assessment parameters like maximum and minimum diameter of the nucleus, cell and perimeter of the cell and nucleus were considered. Results: An increase in maximum and minimum diameter of nucleus, perimeter of nucleus and cell in cases when compared to controls. Conclusions: Fluorosis induces oxidative stress, DNA damage and apoptosis which can be the reasons for the increase in the nuclear size and decrease in the cell size. Community dental and medical programmes should be stringently implemented in fluorosis-endemic areas, to create awareness regarding the toxic effects of fluoride to the body, especially within the oro-facial region.