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Periodontal Disease in Pregnancy Complicated by Type 1 Diabetes Mellitus
Author(s) -
Guthmiller Janet M.,
HassebroekJohnson Jeanne R.,
Weenig Duane R.,
Johnson Georgia K.,
Kirchner H. Lester,
Kohout Frank J.,
Hunter Stephen K.
Publication year - 2001
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2001.72.11.1485
Subject(s) - medicine , diabetes mellitus , gingival margin , pregnancy , periodontal disease , clinical attachment loss , gestation , dentistry , gastroenterology , endocrinology , genetics , biology
Background: Systemic disease and hormonal changes have been implicated as complicating factors for periodontal disease. Diabetes has been identified as a risk factor for periodontal disease, and diabetics can experience periodontal destruction at an earlier age than non‐diabetic individuals. Increased hormone levels during pregnancy can contribute to increased gingival inflammation. The purpose of this study was to examine the association of type 1 diabetes mellitus (DM) on the periodontal status of pregnant women. Methods: Thirty‐three (13 diabetic and 20 non‐diabetic) subjects, 20 to 39 weeks gestation, participated in this study. The mean age of the diabetics and non‐diabetics was 28.5 ± 7.1(SD) and 27.0 ± 7.3 years, respectively. The following parameters were assessed at Ramfjord's reference teeth: plaque index (PI), gingival inflammation (GI), probing depth (PD), gingival margin (GM) location, and clinical attachment level (CAL). Results: Diabetic subjects had significantly ( P <0.001) higher PI (1.48 ± 0.69) and GI (1.77 ± 0.44) scores than non‐diabetics (PI = 0.63 ± 0.38; GI = 0.93 ± 0.48). Mean PD for diabetics (2.95 ± 0.69 mm) was significantly different ( P <0.024) from that of non‐diabetics (2.44 ± 0.32 mm). Although mean GM location was coronal to the cemento‐enamel junction (CEJ) in both groups, gingival margins were at a more apical position ( P <0.001) in the diabetics (−0.20 ± 1.24 mm) compared to non‐diabetics (−1.76 ± 0.53 mm). Mean CAL values also varied significantly ( P <0.001) between diabetics (2.60 ± 1.54 mm) and non‐diabetics (0.68 ± 0.65 mm). Significant differences were seen for GI ( P <0.001), PD ( P = 0.005), GM location ( P <0.001), and CAL ( P <0.001) when assessing the effect of diabetes and controlling for plaque. When assessing the effect of plaque and controlling for diabetes, the only significant difference was GI ( P = 0.001). Conclusions: The results of this study demonstrate that periodontal inflammation and destruction are increased in pregnant diabetics as compared to non‐diabetic pregnant patients. These findings may have implications for diabetic control and, hence, maternal and fetal outcomes in pregnant diabetic patients. J Periodontol 2001;72:1485‐1490.