RESUMEN
Statement of Problem: Tooth caries is influenced by different biochemical characteristics of saliva. As hydroxyapatite is the main component of enamel, salivary ion activity product for hydroxyapatite [IPHA] as well as alkaline phosphatase may be attributed to dental caries
Purpose: The aim of the present study was to compare salivary buffering capacity, alkaline phosphatase and IPHA of adults according to the dental caries and age
Materials and Method: One hundred and twenty 19 to 44 years old male individuals were divided into four groups according to the dental caries rate and age: group 1: 19-35 years old low dental caries [DMFT <5]; group 2: 19-35 years old high dental caries [DMFT 5<]; group 3: 35-44 years old low dental caries [DMFT <11] and 35-44 years old high dental caries [DMFT 11<]. Five milliliter of unstimulated saliva was collected, and then buffering capacity, the level of alkaline phosphatase activity and IPHA was determined for each sample. Data was analyzed by soft ware SPSS using two way ANOVA, Friedman and Mann-Whitney tests
Results: Mean and standard deviation of buffering capacity of group 1 to 4 was 2.66 +/- 0.54, 2.64 +/- 0.56, 2.70 +/- 0.70 and 2.26 +/- 0.82, respectively. The difference was not significance [p= 0. 305]. Mean and standard deviation of alkaline phosphatase activity of group 1 to 4 was 5.82 +/- 2.91, 5.30 +/- 1.52, 4.77 +/- 1.82 and 4.55 +/- 1.61, respectively. There was no significant difference [p= 0.692]. Mean and standard deviation of IPHA of group 1 to 4 was 29.39 +/- 0.61, 29.51 +/- 0.76, 29.14 +/- 0.56 and 29.75 +/- 0.75, respectively. The difference was significant [p= 0.049]
Conclusion: Based on the results of the present study, buffering capacity and the level of alkaline phosphatase couldn't affect dental caries, independently. However, the higher value of IPHA may be attributed to the higher dental caries rate. Ageing decreases alkaline phosphatase activity
RESUMEN
Global initiative for Chronic Obstructive Pulmonary Disease [Gold] has defined COPD as a disease characterized by airflow limitation that is not fully reversible. COPD is a subset of obstructive lung diseases which also includes cystic fibrosis, bronchitis and asthma. Adenosine deaminase [ADA, E.C.3.5.4.4] converts adenosine to inosine. ADA has two isoenzymes; ADA1 and ADA2. In COPD patients the serum level of ADA increases which can be regarded as a result of reduction in ADA activity. In this study we evaluated the level of ADA and its isoenzymes in COPD patients and healthy subjects. This was a case control study. ADA activity in 30 COPD patients with age range of 20-60 years whose disease had been confirmed by a pulmonologist in Ekbatan Hospital, was compared to the activity of the same enzyme in 60 healthy subjects consisting of 30 non smoker and 30 smoker subjects as control groups. Data were introduced into SPSS version.13 software and analyzed by Kruskall-Wallis and two-way ANOVA tests. ADA activity in the COPD and smoker control groups was significantly lower than that of non smoker group [18.99 +/- 7 and 22.99 +/- 6.7 U/L, respectively]. Regarding ADA2 serum level, the difference between patient group and non smoker control group was significant [P<0.05]. Activity of ADA1 isoenzyme in the study groups did not show any significant differences. In general ADA activity was decreased in COPD patients. Decreased ADA activity together with increased adenosine level may play an important role in producing pulmonary damage in COPD patients