Background: Chronic periodontitis is an inflammatory disease that affects the supporting tissues of the teeth and it’s common among adults. Smoking is an important risk factor for periodontitis induces alveolar bone loss. Alkaline phosphatase enzyme is involved in the destruction of the human periodontium. It is produced by many cells such as polymorphonuclear leukocytes, osteoblasts, macrophages and fibroblasts within the area of the periodontium and gingival crevice. Osteocalcin is one of the most abundant matrix proteins found in bones and the only matrix protein synthesized exclusively there. Smaller Osteocalcin fragments are found in areas of bone remodeling and are actually degradation products of the bone matrix.The purpose of this study was to evaluatethe effect of smoking on the salivary 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) were obtained from study groups (25 light smokers and 33 non-smokerssubjects, both with chronic periodontitis) and control groups (8 light smokers and 13 non-smokers subjects, both with healthy periodontium). All subjects were systemically healthy males, with age range (30-50) years. Salivary Alkaline phosphatase and Osteocalcin levels were determined by Colorimetric and Enzyme-linked Immunosorbent Assays, respectively. Results: Smoker chronic periodontitis patients revealed non-significant differences in clinical periodontal parameters with 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 chronic periodontitis group, while there were highly significant differences in terms of Gingival index and Bleeding on probing(P ≤ 0.01).Osteocalcin levels were lower in smoker chronic periodontitis group (0.13±0.20) than non-smoker chronic periodontitis group (1.09±2.26) with significant difference (0.05 ≥ P > 0.01). Mean of Alkaline phosphatase level was lower in smoker chronic periodontitis (11.14±4.53) than non-smoker chronic periodontitis (11.45±4.17) with a non-significant difference, while there was a significant difference inAlkaline phosphatase concentrations between smoker and non-smoker control groups.There were non-significant differences between smoker chronic periodontitis and smoker control groups in terms of Osteocalcin and Alkaline phosphatase concentrations. There were non-significant differences between non-smoker chronic periodontitis and non-smoker control groups in terms of Osteocalcin and Alkaline phosphatase concentrations. Conclusion: Within the limits of this study, it may be suggested that suppression of salivary Osteocalcin levels by smoking and slight increase in alkaline phosphatase in smokers groups, may explain the deleterious effects of smoking on periodontal health status.