In the present two-year longitudinal investigation, the progression of periodontal disease was assessed after 1 year from the baseline examination in 38 dentate subjects and after 2 years in 22 dentate subjects with a mean duration of 18 years of insulin-dependent diabetes mellitus. The diabetics, aged 35 to 56 years at baseline, were under medical treatment at the outpatient clinic of the III Department of Medicine, University Central Hospital of Helsinki and at 2 diabetic clinics of the Helsinki Health Centre. Based upon their long-term medical records, 26 subjects were at baseline identified as having poorly controlled insulin-dependent diabetes (PIDD) with a mean blood glucose level of 12.5 mmol/l and a mean glycosylated hemoglobin (HBA1) level of 10.1%. 12 subjects were classified as having controlled insulin-dependent diabetes (CIDD) with a mean blood glucose level of 6.7 mmol/l and a mean HBA1 level of 9.2% at baseline. For each individual, recordings were made at baseline and after 1 and 2 years from the baseline for the plaque index, gingival index, pocket depth, loss of attachment, bleeding after probing, gingival recession, and radiographic loss of alveolar bone. At baseline and 2 years after the baseline examination, the PIDD subjects had similar plaque conditions as the CIDD subjects. At baseline and after 1 and 2 years from baseline the PIDD subjects had more gingivitis and bleeding after probing (P < 0.05, chi 2-test) than the CIDD subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present site-by-site follow-up study, the change in amount of approximal alveolar bone was assessed after 1 year from the baseline examination in 38 and after 2 years in 22 dentate subjects all with insulin-dependent diabetes mellitus. The diabetics, aged 35 to 56 years at baseline, had a history of a mean duration of 18 years of insulin-dependent diabetes mellitus and were under medical treatment at the outpatient clinic of the III Department of Medicine, University Central Hospital of Helsinki as well as at 2 diabetic clinics of the Helsinki Health Centre. Based upon their long-term medical records, 26 subjects were after 1 year, and 16 subjects after 2 years from the baseline, identified as having poorly controlled insulin-dependent diabetes (PIDD). At the 1-year examination, 12 subjects were classified as having controlled insulin-dependent diabetes (CIDD) as compared to 6 subjects at the 2-year examination. After 1 and 2 years, from baseline, site-by-site measurements were recorded for plaque index scores, bleeding after probing, loss of attachment, and radiographic loss of alveolar bone. After 1 and 2 years from baseline, the PIDD subjects exhibited higher mean %s of sites with improved bleeding scores (P < 0.01, chi 2-test) than the CIDD subjects. At the 2-year examination, the mean % of sites with loss of approximal alveolar bone was greater in the PIDD than in the CIDD group (P < 0.05, chi 2-test). The greatest differences between PIDD and CIDD subjects were found when recordings for only canines were analyzed at the 1- and 2-year examinations (P < 0.05, chi 2-test). The results of our current 2-year longitudinal site-by-site examinations confirm earlier results that poorly controlled insulin-dependent diabetes mellitus is strongly related to the amount of alveolar bone loss.

This study examined cellular and vascular changes in gingival connective tissue samples by stereologic point-counting procedures and interactive digital analyzing systems in long-term insulin-dependent diabetes mellitus patients. Gingival connective tissue capillaries representing a clinically healthy sulcus with no evidence of periodontal disease at the site of biopsy were studied in 29 patients with diabetes. Based upon their long-term medical records, 19 were identified as having poorly controlled (PIDD) and 10 as controlled insulin-dependent diabetes mellitus (CIDD). Ten nondiabetic, age- and gender-matched individuals served as controls. Thirty-nine biopsies were processed for light microscopy, and the blood vessel area was analyzed using an interactive digital analyzing system; 9 gingival biopsies, 5 diabetic and 4 controls, were processed for morphometric electron microscopic analysis. For each individual, site-specific recordings were made for the plaque index, bleeding index, probing depth, loss of attachment, and radiographic loss of interproximal alveolar bone. No evident signs of periodontitis occurred at the biopsy sites. For each PIDD patient, respective volumetric and numeric densities of cellular components including fibroblasts, neutrophilic granulocytes, monocyte/macrophages, mast cells, lymphocytes, blast cells, and plasma cells were recorded in the inflamed connective tissue (ICT). Non-cellular components such as collagen fibers and blood vessels were also recorded. PIDD patients had elevated plasma cell levels relative to controls and they appeared also to have a decreased collagen fiber density. In addition, fibroblasts occupied less volume in the ICT of PIDD patients than in controls. PIDD patients had the largest mean area of cross-section of the blood vessels, but this difference was not statistically significant (P > or = 0.211; t-test). No specific characteristics of ICT or vascular changes were detectable in adult well-controlled long-term diabetics under similar plaque conditions. Swollen and proliferated endothelial cells were frequently found in PIDD patients and the mean distance from the lumen to the outer border of basement membrane was greater in the PIDD than in the controls (P < 0.001; t-test). Overall, our findings that cellular, vascular, and connective tissue changes indicative of increased catabolism rather than anabolism detected in gingiva are especially associated with poorly controlled long-term insulin-dependent diabetes.

The subgingival microflora was assessed by means of dark field microscopy in 106 pockets of 47 subjects with long-term insulin-dependent diabetes mellitus (IDD). The microbiota of 55 healthy sulci (probing depth < 4 mm) and 51 periodontally diseased (probing depth > or = 4 and 6 mm) pockets were analyzed. The mean duration of the IDD of the diabetic subjects was 23.7 years (range from 10 to 41 years). The diabetic patients, aged 30-65 years, were under medical treatment at the III Department of Medicine, University of Helsinki Central Hospital, and at 2 clinics of the Helsinki Health Centre. Based upon their long-term medical records, 26 subjects were assessed to have poorly controlled insulin-dependent diabetes mellitus (PIDD) and 21 had controlled insulin-dependent diabetes (CIDD). The PIDD subjects exhibited higher mean blood glucose levels (12.9 +/- 4.6 mmol/l, mean +/- S.D.) than the CIDD subjects (7.9 +/- 3.6 mmol/l) (p < 0.001, t-test). The mean glycosylated hemoglobin HBA1 (HBA1c) levels were 11.2 +/- 4.6% (10.3 +/- 1.2%) and 8.8 +/- 1.8% (7.7 +/- 1.4%) for PIDD and CIDD subjects, respectively. These differences were statistically significant (p < 0.01 and p < 0.001, t-test). For each individual, site-specific recordings were made for plaque index and bleeding index scores, probing depth, loss of attachment and radiographic loss of alveolar bone. Dark field microscopy analysis of the presence of spirochetes, motile rods, cocci, non-motile rods, filaments and fusiforms was performed in the total of 106 pockets. According to the results of the dark field microscopy, the % of spirochetes and motile rods in the periodontally diseased pockets was significantly higher in the PIDD than in the CIDD subjects (9.2 +/- 13.4% and 10.8 +/- 14.3% versus 4.0 +/- 5.2% and 3.1 +/- 3.2%, p < 0.01 and p < 0.001, chi 2-test, respectively). Moreover, the PIDD subjects had lower mean %s of coccoid cells in periodontally diseased sites than the CIDD subjects (52.1 +/- 20.8% versus 60.7 +/- 9.0%, p < 0.001, chi 2-test).