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.
This study investigates the impact of nonsurgical periodontal treatment (NSPT) on oral health-related quality of life (OHRQoL) in patients with periodontitis stages (S)2 and S3, and the factors associated with the prediction of patient-reported outcomes. Periodontitis patients (n = 68) with moderately deep periodontal pockets were recruited. Responses to the Oral Health Impact Profile (OHIP)-14 questionnaire and clinical parameters including plaque index, bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment loss (CAL) were recorded. All patients received supra- and subgingival professional mechanical plaque removal. All clinical parameters and questionnaire responses were recorded again 3 months after NSPT.
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In vivo study revealed that ZnO nanoparticles treatment of Streptococcus SPP contaminated injured skin showed good prognosis and good healing process include complete regeneration of the epithelial cells of the epidermis and increase of cellulartiy of the dermal content compared with untreated group. In conclusion, treatment of S. pyogenes infected skin with Zinc oxide nanoparticles concentration (2 mg/ml) limit the skin damage and localized the lesion to the incision site with good healing process
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The study included a statement toxicity of some heavy metals individually and collectively and the existence of plant nutrients in the center Agirenk bluish green moss growth and Askhaddm biomass as an indicator of the study, in addition to portability moss on the accumulation of the metal
Background: CYP1A1 gene polymorphisms and tobacco smoking are among several risk factors for various types of cancers, but their influence on breast cancer remains controversial. We analyzed the possible association of CYP1A1 gene polymorphisms and tobacco smoking-related breast cancer in women from Iraq. Materials and methods: In this case-control study, gene polymorphism of CYP1A1 gene (CYP1A1m1, T6235C and CYP1A1m2, A4889G) of 199 histologically verified breast cancer patients' and 160 cancer-free control women's specimens were performed by using PCR-based restriction fragment length polymorphism. Results: Three genotype frequencies (TT, TC, and CC) of CYP1A1m1T/C appeared in 16.1, 29.6, and 54.3% of women with breast cancer, respectiv
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Systemic lupus Erythematosus is an autoimmune disease of unknown aetiology affecting multiple organ system. Reactive nitrogen and oxygen species are claimed to play a role in this disease. However, the potential of Nitrosative/Oxidative Stress to elicit an autoimmune, response remain till now largely unexplored in humans. This study was done to investigate the status and contribution of nitrosative/oxidative stress in Iraqi patients for systemic lupus erythematosus. Blood samples from 19 patients with systemic lupus erythematosus and 19 age-and sex- matched apparently healthy controls were evaluated for serum levels of nitrosative/oxidative stress markers including nitric oxide, peroxynitrite and malondialdehyde. Nitric oxide levels were
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Background: Pregnancy is considered a major risk factor for development and progression of periodontal disease. There are hormonal changes in both estrogen and progesterone hormones in addition to bacterial effect and poor oral hygiene that will enhance development of periodontal disease in pregnant women. Materials and methods: Seventy subjects were enrolled in the study, the subjects with an age range (20-35) years old without any history of systemic disease. The subjects were divided into 20 non-pregnant women they represent the control group (G I), 30 pregnant women with gingivitis (GII) and 20 pregnant women with periodontitis (GIII).All periodontal parameters (plaque index, gingival index, bleeding on probing, probing pocket depth an
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