ABSTRACT
Background: Periodontitis involves intricate interactions of the biofilm with the host immunoinflammatory response and subsequent alterations in bone and connective tissue homeostasis. Neopterin is a marker, belonging to the class of pteridines, which is associated with cell-mediated immunity. It is produced by interferon-γ stimulated macrophages. The levels of neopterin in body fluids are elevated in infections, autoimmune diseases, malignancies and allograft rejections. This investigation was designed to estimate the levels of neopterin in gingival crevicular fluid (GCF) in health, chronic gingivitis and chronic periodontitis. Materials and Methods: Thirty subjects were divided into three groups of ten subjects each as with healthy periodontium (Group 1), chronic gingivitis (Group 2) and chronic periodontitis (Group 3). The GCF samples were obtained from the subjects by placing color-coded calibrated, volumetric, micro-capillary pipettes extracrevicularly. The samples were placed in plastic vials and stored at −70°C until the time of neopterin estimation using enzyme immunoassay. Results: The mean neopterin level in Group 3 (126.28 ± 37.70 nmol/L) is significantly higher than the mean neopterin level in Group 1 (48.66 ± 18.82 nmol/L) and Group 2 (70.68 ± 18.26 nmol/L) (P < 0.05). However, there is no significant relationship between neopterin levels and various clinical parameters in each study group (P > 0.05). Conclusions: The results of our study indicate that the neopterin levels in GCF are positively associated with periodontal disease, which may provide a useful tool in monitoring its progression. Nevertheless, further longitudinal studies are required with larger sample sizes in which neopterin levels are progressively estimated and compared to baseline values.
ABSTRACT
Background: Drug-induced gingival overgrowth (DIGO) is one of the unwanted side effects of amlodipine therapy, but the pathogenesis still remains unclear. Apoptosis, which plays a ubiquitous role in tissue homeostasis, including gingiva, may be involved in the development of gingival enlargement. Aims and Objectives: (i) To study the distribution of Bcl-2 in healthy and overgrown gingival tissues. (ii) To compare and correlate the Bcl-2 expression in gingival samples from subjects on amlodipine therapy to the findings in healthy controls. Materials and Methods: A total of 25 subjects were recruited for the study - 15 hypertensive patients and 10 systemically healthy subjects. Both the groups were analyzed for Bcl-2 expression using immunohistochemistry. Results: Few of the control specimens showed weak positivity to Bcl-2 antibody, with the distribution limited to the basal cell layers alone, whereas 10 hyperplastic specimens expressed Bcl-2 and, unlike the control group, the distribution pattern was seen in both basal and suprabasal layers. Conclusion: The results indicate that the pathogenesis of amlodipine-induced gingival overgrowth might involve inhibition of apoptosis, especially with morphogenesis of hyperplastic gingival epithelia.