The effect of diabetes mellitus on bone metabolism and bone mineral density is discussed controversially. Diabetes mellitus due to an autoimmune process seems to be associated with low turnover osteopenia either in the animal model or in children and adolescents. A number of factors are discussed as being involved, but in this age group clinical symptoms are missing. Adult patients of either sex with IDDM show a reduced bone mineral density when measured at peripheral sites such as the distal forearm or the femoral neck, diabetic complications such as neuropathy and microangiopathy seem to pronounce the deficit of bone mass. In these patients, osteopenia is accompanied by a high turnover situation of bone metabolism, possibly due to microvascular complications. In contrast, patients with NIDDM and here especially overweight women have a normal or even increased bone mineral density. Up to now, there is no convincing evidence for an increased incidence of osteoporotic fractures in diabetic patients. Systemic diabetic osteopenia therefore does not seem to be of great epidemiological relevance.

Our results support previous findings that BMD is subnormal in adults with GHD, that GH replacement therapy can stimulate bone turnover in such adults and that, in the long term, such stimulation results in a significant increase in BMD. In addition they show, for the first time, that BMD may continue to rise even after GH replacement therapy has been administered for 4 years, and indicate that bone elasticity is not adversely affected by long-term GH therapy.

Hypercortisolism and glucocorticoid treatment, even in a low dose or administered topically, may influence bone metabolism. It was the aim of this study to investigate whether there might be differences in the regulation of endogenous cortisol secretion between patients with established primary vertebral osteoporosis and healthy controls. Suppressed morning serum cortisol concentrations in a 3 mg dexamethasone overnight suppression test were compared in well-defined healthy postmenopausal women (n = 149) and osteoporotic patients classified as having established primary vertebral osteoporosis with no clinical features of hypercortisolism (n = 78). Suppressed cortisol in the healthy controls was 1.08 +/- 0.44 microg/dl and in the primary osteoporotics 1.58 +/- 1.42 microg/dl (p < 0.0001). Of the investigated primary osteoporotics 15.4% (n = 12) had suppressed cortisol levels above the 97.5th percentile (1.96 microg/dl) of the healthy controls. Subgroup analysis regarding the influence of gonadal steroid hormone replacement in both groups and gender in the osteoporotic group did not change the results. Four of the 12 patients with incomplete suppressive cortisol underwent adrenal endosonography, unilateral adrenal nodular hyperplasia being detected in three cases. In two patients the diagnosis was confirmed by histology and normalisation of a dexamethasone suppression test following endoscopic adrenalectomy. These data yield evidence for a difference in the regulation of cortisol secretion following high-dose dexamethasone administration between healthy subjects and a subgroup of patients with primary osteoporosis. This might be due to a relevant amount of autonomous cortisol secretion in some of these patients; however, even cortisol resistance has to be taken into account.

The square of ultrasound transmission velocity in a material is related to the modulus of elasticity, which is known to be an indicator of stability in bone. The aim of our study was to use ultrasound transmission velocity to obtain information about the material properties of bone tissue, keeping other factors possibly influencing ultrasound transmission as constant as possible. Apparent phalangeal ultrasound transmission velocity (APU) measured in 54 isolated, fresh pig phalanges was shown to be independent of bone mineral density (BMD) measured by SPA. Fastest sound transmission led exclusively through cortical bone so that intertrabecular connectivity in spongious bone could not influence the result. In humans APU was measured in the mediolateral direction at the midphalanx of the middle finger. In 53 healthy subjects (15-81 years old; 27 women, 26 men), there was a decrease of APU with age (r = -0.30, p < 0.05). Further, when comparing the results of both hands intraindividually almost identical values indicated constant intraindividual architecture of bone at this location. There was no evidence for a relation of APU to physical load comparing dominant and nondominant hand and relating the results to subjectively estimated physical load. In a second group of 43 perimenopausal women (47-60 years old), APU, which again decreased with age (r = -0.33, p < 0.05), was found not to be correlated to BMD measured by SPA at the distal forearm (cortical bone).(ABSTRACT TRUNCATED AT 250 WORDS)

In a number of endocrine disorders, typical changes in skin thickness can be observed which make measurement of skin thickness interesting in this field. A newly developed mechanical method for measuring skin thickness is presented. Using a digital measuring screw on the dorsum of the hand with a defined measuring force of 10 newton and a resulting tissue compression of 1500 mm Hg, highly reproducible results were obtained (mean coefficient of variation 2.56%). In 129 women, 37 to 78 years old, body mass index < 30 kg/m2, there was no significant relation between body mass index and skin fold thickness. A negative correlation between skin fold thickness and age (r = 0.37, p < 0.001) was detected. This has been shown for skin by other methods previously and is well known to occur in bone, another tissue whose matrix as well as dermis consists mainly of collagen type I. In 30 subjects, half hypopituitary patients, half healthy subjects (17 women, 13 men; 43.3 +/- 10.5 years old), skin fold thickness measured mechanically and sonographically determined skin thickness correlated with r = 0.46 (p < 0.01). A significant correlation between bone mineral density measured by single photon-absorptiometry at the ultradistal forearm and skin fold thickness measured mechanically was found and skin fold thickness measured mechanically was found (r = 0.36, p < 0.05), whereas this was not the case for sonographically determined skin thickness and bone mineral density (r = 0.13, n.s.). This newly developed method might be useful in clinical studies on endocrine disorders affecting skin (and bone) metabolism and the regulation of collagen type I metabolism in general.