Urea Levels in the Gingival Crevices of Diabetic and Normal Adolescents
Urea Levels in the Gingival Crevices of Diabetic and Normal Adolescents
复制标题
糖尿病和正常青少年牙龈缝隙中的尿素水平
DOI：
10.1177/00220345770560100201
复制
发表时间：
1977
影响因子：
7.6
通讯作者：
I. Kleinberg
中科院分区：
文献类型：
--
作者：
S. Ciancio;L. Golub;L. Mosovich;C. Katz;I. Kleinberg
The present study has determined whether urea, shown to exist in high concentration in the GCF (gingival crevicular fluid) of healthy individuals (GOLUB et al., J Periodont Res 6:243, 1971), is elevated in the GCF of diabetics and might, like glucose, be an earlier indicator of systemic disease. Using filter paper strips, GCF was collected from 8 diabetics and 8 normal subjects between 11 and 14 years of age. Each diabetic subject was assessed by a physician (L.M.) as having moderately severe diabetes and had been diagnosed as diabetic for 7.4 + 0.4 (S.D.) years. All diabetics received daily injections of insulin and diet counseling. GCF volume and urea content were measured as described previously (GOLUB et al. 1971). The GCF glucose collected on filter paper strips was measured with a standard ultramicro method (Fundamentals of Clinical Chem., ed. N. TIETZ, 1976, W. B. Saunders & Co., p 245). The sites sampled, 8 to 10 in each subject, were the proximal crevices of the maxillary and mandibular incisors. All were instructed to avoid oral hygiene procedures and not to eat for 12 hours before fluid collection which was always between 8:00 and 10:00 a.m. After sampling for GCF, gingival inflammation was scored according to the method of LOE and SILNESS (Acta Odonto Scand 21:533, 1963); pocket depth was measured with standardized Williams-Fox periodontal probes and blood was sampled for glucose analysis. The results are shown in the table. The two groups were similar in age, severity of gingival inflammation, and flow of GCF. The adolescent diabetics showed much higher fasting blood and GCF glucose concentrations (P < 0.01) and slightly shallower pockets (P < 0.01) FICARA et al. (J Periodont Res 10:171, 1975) found a similar difference in older diabetic and normal subjects (mean age 45 years) with slightly deeper pockets (mean depth for normal subjects, 3.5 mm; for diabetics, 2.9 mm). Despite similarity in GCF flow, the crevicular fluid of the diabetic subjects contained more urea. Most (77%) GCF samples in this study came from gingivae with a gingival index of 1; the remaining samples came from tissues with an index of 2 or 3. Although GCF urea concentration in both normal and diabetic subjects was found to be inversely related to the severity of inflammation, the diabetics showed higher GCF urea concentrations at all three levels of gingival inflammation. The relationship between GCF urea concentration and severity of gingival inflammation in the normal subjects was almost identical with that reported previously (GOLUB et al., 1971). It would appear that urea levels, like glucose levels, are elevated in the diabetic and might be useful in the diagnosis of this and possibly other systemic diseases. The elevated GCF urea levels might be expected, from earlier studies, to favor more ammonia formation, a higher pH, and increased gingival disease (GOLUB and KLEINBERG, 1976). However, a complicating factor in the diabetic is the elevated glucose concentration in the GCF (FICARA et al., 1975) which could counteract some of the effects of urea by inhibiting ammonia formation and reducing the pH. Ammonia at alkaline pH appears to be a tissue irritant (LEVEEN et al., Ann Surg 178: 745, 1973) and glucose could reduce both by diverting urea metabolism in the bacteria away from ammonia formation and into amino acid synthesis (BISWAs and KLEINBERG, Arch Oral Biol 16:759, 1971). The long-term effects of elevated levels of both glucose and urea in the GCF on the crevicular microflora and in turn on the periodontal tissues remains to be determined, but once elucidated might clarify the pathogenesis of periodontal disease in diabetics.
