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Aim:Vitamin D is associated with inflammatory diseases such as periodontal disease and diabetes mellitus (DM). The aim of our study was to find out the level of serum Vitamin D in chronic periodontitis patients (CHP) with and without type 2 DM.Materials and Methods:This study consists of 141 subjects, including 48 controls. Case groups consisted of 43 chronic periodontitis patients with type 2 DM (CHPDM) and 50 CHP. pocket depth (PD), clinical attachment loss (CAL), modified gingival index (MGI), plaque index (PI), and calculus index (CI) were taken. Serum 25-hydroxyvitamin D (25[OH] D) level in ηg/ml was estimated by electrochemiluminescence immunoassay with Elecsys and cobase e immunoassay analysers(cobase e 411). Other laboratory investigations including fasting blood sugar (FBS) and serum calcium were measured in all subjects.Results:The mean serum 25(OH) D level was 22.32 ± 5.76 ηg/ml, 14.06 ± 4.57 ηg/ml and 16.94 ± 5.58 ηg/ml for control, CHPDM and CHP groups respectively. The difference was statistically significant (P < 0.05). The mean value of FBS was significantly high in CHPDM group as compared to CHP group. Periodontal parameters like MGI, PI, PD, and CI showed significant difference between groups (P < 0.05) and higher score was found in CHP group, while CAL and PI showed no statistically significant difference between CHP and CHPDM group (P > 0.05).Conclusions:This study observed a low level of serum Vitamin D level in patients with CHP and CHPDM. Low Vitamin D level was observed in case groups may be due to the diseases process rather than low Vitamin D acting as a cause for the disease.

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Pedigree analysis of the oral cancer (OC) patients registered at our Centre had disclosed familial aggregation of oral cancer which hitherto has not been largely reported. There is a paucity of information on the genetic determinism for familial oral cancer predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin-induced chromosome sensitivity of 7 familial and 10 sporadic oral cancer patients and 14 unaffected family members (first-degree relatives) to determine whether these factors could give any clues regarding cancer-predisposing factors. Neither the oral cancer patients nor the unaffected family members showed any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the oral-cancer patients and unaffected relatives. The mean b/c value was I .68 f 0.48 for familial OC patients, I. I 2 f 0.36 for sporadic OC patients and 0.52 f 0. I 8 for the unaffected family members (p < 0.00 I). A noteworthy observation was that one unaffected family member also showed bleomycin hypersensitivity and expressed a mean b/c value of I .32, at the initiation of the study. That patient later developed oral carcinoma. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in OC families may be related to cancer predisposition. The mutagen sensitivity study is being continued in a larger series of subjects, for the development of a cytogenetic marker for prediction of cancer susceptibility.8 1996 Wiley-Liss, Inc.

Pedigree analysis of the oral cancer (OC) patients registered at our Centre had disclosed familial aggregation of oral cancer which hitherto has not been largely reported. There is a paucity of information on the genetic determinism for familial oral cancer predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin-induced chromosome sensitivity of 7 familial and 10 sporadic oral cancer patients and 14 unaffected family members (first-degree relatives) to determine whether these factors could give any clues regarding cancer-predisposing factors. Neither the oral cancer patients nor the unaffected family members showed any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the oral-cancer patients and unaffected relatives. The mean b/c value was I .68 f 0.48 for familial OC patients, I. I 2 f 0.36 for sporadic OC patients and 0.52 f 0. I 8 for the unaffected family members (p < 0.00 I). A noteworthy observation was that one unaffected family member also showed bleomycin hypersensitivity and expressed a mean b/c value of I .32, at the initiation of the study. That patient later developed oral carcinoma. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in OC families may be related to cancer predisposition. The mutagen sensitivity study is being continued in a larger series of subjects, for the development of a cytogenetic marker for prediction of cancer susceptibility.8 1996 Wiley-Liss, Inc.