Nuclear abnormalities in buccal mucosa cells of patients with type I and II diabetes treated with folic acid.

Diabetes mellitus (DM) is characterized by high blood glucose. Excessive production of free radicals may cause oxidative damage to DNA and other molecules, leading to complications of the disease. It may be possible to delay or reduce such damage by administration of antioxidants such as folic acid (FA). The objective of this study was to determine the effect of FA on nuclear abnormalities (NAs) in the oral mucosa of patients with DM. NAs (micronucleated cells, binucleated cells, pyknotic nuclei, karyorrhexis, karyolysis, abnormally condensed chromatin, and nuclear buds) were analyzed in 2000 cells from 45 healthy individuals (control group) and 55 patients with controlled or uncontrolled type I or II DM; 35 patients in the latter group were treated with FA. Samples were taken from the FA group before and after treatment. An increased rate of NAs was found in patients with DM in comparison with that of the control group (P<0.001). FA supplementation in patients with DM reduced the frequency of NAs (20.4 ± 8.0 before treatment vs. 10.5 ± 5.2 after treatment; P<0.001). The type I and type II DM and controlled and uncontrolled DM subgroups were analyzed in terms of sex, age, and smoking habit. The significantly reduced frequencies of buccal mucosa cells with micronuclei, binucleation, pyknosis, karyorrhexis, karyorrhexis+abnormally condensed chromatin, karyolysis, and nuclear buds produced by FA supplementation in DM patients (P<0.02) are consistent with the idea that free radicals are responsible for the increased frequency of NAs in DM patients.

Increased micronuclei and nuclear abnormalities in buccal mucosa and oxidative damage in saliva from patients with chronic and aggressive periodontal diseases.

BACKGROUND AND OBJECTIVE: Periodontal disease is a chronic bacterial infection characterized by connective tissue breakdown and alveolar bone destruction because of inflammatory and immune response caused by periodontopathogens and long-term release of reactive oxygen species. A high number of reactive oxygen species result in periodontal tissue damage through multiple mechanisms such as lipid peroxidation, protein denaturation and DNA damage. The aim of this study was to evaluate DNA and oxidative damage in subjects with chronic or aggressive periodontitis and healthy controls. MATERIAL AND METHODS: Buccal mucosa cells and whole saliva were collected from 160 subjects, who were divided into three groups: subjects with chronic periodontitis (CP) (n = 58), subjects with aggressive periodontitis (AgP) (n = 42) and a control group (n = 60). DNA damage was determined by counting micronuclei (MN) and nuclear abnormalities (NAs) in exfoliated cells, including binucleated cells, cells with nuclear buds and karyolitic, karyorrhectic, condensed chromatin and pyknotic cells. The degree of oxidative stress was determined by quantifying 8-hydroxy-2'-deoxyguanosine (8-OHdG) in whole saliva. RESULTS: Subjects with CP or AgP presented significantly more ( p < 0.05) MN and NAs and higher levels of 8-OHdG ( p < 0.05) compared with the control group. CONCLUSION: Our results indicate that subjects with periodontitis (CP or AgP) exhibited an increase in the frequency of MN, NAs and 8-OHdG, which is directly related to DNA damage. In addition, a positive correlation exists between oxidative stress produced by periodontitis disease and MN.

IL-12 and IL-18 levels in serum and gingival tissue in aggressive and chronic periodontitis.

OBJECTIVE: The aim of this study was to compare the levels of interleukin-12 (IL-12) and IL-18 in gingival tissue and serum between patients with chronic (n = 18) or aggressive periodontitis (n = 12) and healthy subjects (HS) (n = 9). METHODS: Gingival tissue biopsies and serum were obtained from all study subjects. The tissue was homogenized and cytokines IL-12 and IL-18 were quantified by enzyme-linked immunosorbent assay. RESULTS: Interleukin-12 levels in gingival tissue were significantly higher in aggressive periodontitis patients than in HS; serum IL-12 was significantly elevated in aggressive periodontitis relative to both chronic periodontitis (CP) and HS. IL-18 levels in gingival tissue showed no significant differences between the groups. Patients with CP showed significantly elevated levels of serum IL-18 compared with HS; however, the aggressive periodontitis group showed no significant differences with either the CP group or the HS. CONCLUSIONS: Our results showed higher levels of IL-12 in gingival tissue and serum of patients with aggressive periodontitis, and IL-18 was elevated in the serum of CP patients. The patterns of IL-12 and IL-18 are different in chronic and aggressive periodontitis; this finding suggests distinctive mechanisms of immunopathogenesis between these forms of periodontitis.