Effects of light smoking on salivary levels of alkaline phosphatase and osteocalcin in chronic periodontitis patients

Abstract

Background: Chronic periodontitis is an inflammatory disease that affects the supporting tissues of the teeth and it’scommon among adults. Smoking is an important risk factor for periodontitis induces alveolar bone loss. Alkalinephosphatase enzyme is involved in the destruction of the human periodontium. It is produced by many cells such aspolymorphonuclear leukocytes, osteoblasts, macrophages and fibroblasts within the area of the periodontium andgingival crevice. Osteocalcin is one of the most abundant matrix proteins found in bones and the only matrix proteinsynthesized exclusively there. Smaller Osteocalcin fragments are found in areas of bone remodeling and are actuallydegradation products of the bone matrix.The purpose of this study was to evaluatethe effect of smoking on thesalivary alkaline phosphatase and Osteocalcin in subjects with chronic periodontitis compared to control subjects.Materials and Methods: Five ml of unstimulated whole saliva samples and full-mouth clinical periodontal recordings(plaque index, gingival index, bleeding on probing, probing pocket depth and clinical attachment level) wereobtained from study groups (25 light smokers and 33 non-smokerssubjects, both with chronic periodontitis) andcontrol groups (8 light smokers and 13 non-smokers subjects, both with healthy periodontium). All subjects weresystemically healthy males, with age range (30-50) years. Salivary Alkaline phosphatase and Osteocalcin levels weredetermined by Colorimetric and Enzyme-linked Immunosorbent Assays, respectively.Results: Smoker chronic periodontitis patients revealed non-significant differences in clinical periodontal parameterswith non-smoker counterparts (P o.o5) in terms of Plaque index, Probing pocket depth and Clinical attachment loss,with slight increase in plaque index value in smoker chronic periodontitis group(1.42±0.46) than non-smoker chronicperiodontitis group, while there were highly significant differences in terms of Gingival index and Bleeding onprobing(P ≤ 0.01).Osteocalcin levels were lower in smoker chronic periodontitis group (0.13±0.20) than non-smokerchronic periodontitis group (1.09±2.26) with significant difference (0.05 ≥ P > 0.01). Mean of Alkaline phosphataselevel was lower in smoker chronic periodontitis (11.14±4.53) than non-smoker chronic periodontitis (11.45±4.17) with anon-significant difference, while there was a significant difference inAlkaline phosphatase concentrations betweensmoker and non-smoker control groups.There were non-significant differences between smoker chronic periodontitisand smoker control groups in terms of Osteocalcin and Alkaline phosphatase concentrations. There were nonsignificantdifferences between non-smoker chronic periodontitis and non-smoker control groups in terms ofOsteocalcin and Alkaline phosphatase concentrations.Conclusion: Within the limits of this study, it may be suggested that suppression of salivary Osteocalcin levels bysmoking and slight increase in alkaline phosphatase in smokers groups, may explain the deleterious effects ofsmoking on periodontal health status.