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Sowohl der Diabetes mellitus als auch die Osteoporose sind chronische Erkrankungen, die auf Grund Ihrer Häufigkeit eine sehr hohe soziale und medizinische Bedeutung haben. Eine Bewertung der Beziehung zwischen Osteoporose- und DM-Risiko ergab, dass ein hohes und sehr hohes Risiko für Diabetes mellitus mit einem hohen und sehr hohen Risiko für die Entwicklung von Osteoporose kombiniert ist (Drobot et al., 2010). Bei hoher Hyperglykämie und Insulininsuffizienz verschlechtern sich die Mineralisierungsprozesse des Knochengewebes und die Synthese von Protein und Kollagen, was sich negativ auf die Prozesse der Knochenbildung auswirkt. Trotz der bedeutenden Fortschritte bei der Erforschung der Ätiologie und Pathogenese sind die detaillierte Wirkung des DM auf die Mineralzusammensetzung des Knochengewebes nach wie vor unklar (Hofbauer et al., 2007). Somit war es das Hauptziel der vorliegenden Untersuchungen, die strukturellen Veränderungen und die Veränderungen der Mineralzusammensetzung im Knochengewebe im Zusammenhang mit dem DM am etablierten Streptozotocin-Diabetes-Modell der Ratte zu analysieren.

Hyperthyroidism causes secondary osteoporosis through favoring bone resorption over bone formation, leading to bone loss with elevated bone fragility. Osteocytes that reside within lacunae inside the mineralized bone matrix orchestrate the process of bone remodeling and can themselves actively resorb bone upon certain stimuli. Nevertheless, the interaction between thyroid hormones and osteocytes and the impact of hyperthyroidism on osteocyte cell function are still unknown. In a preliminary study, we analyzed bones from male C57BL/6 mice with drug-induced hyperthyroidism, which led to mild osteocytic osteolysis with 1.14-fold larger osteocyte lacunae and by 108.33% higher tartrate-resistant acid phosphatase (TRAP) activity in osteocytes of hyperthyroid mice compared to euthyroid mice. To test whether hyperthyroidism-induced bone changes are reversible, we rendered male mice hyperthyroid by adding levothyroxine into their drinking water for 4 weeks, followed by a weaning period of 4 weeks with access to normal drinking water. Hyperthyroid mice displayed cortical and trabecular bone loss due to high bone turnover, which recovered with weaning. Although canalicular number and osteocyte lacunar area were similar in euthyroid, hyperthyroid and weaned mice, the number of terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling (TUNEL)-positive osteocytes was 100% lower in the weaning group compared to euthyroid mice and the osteocytic TRAP activity was eightfold higher in hyperthyroid animals. The latter, along with a 3.75% lower average mineralization around the osteocyte lacunae in trabecular bone, suggests osteocytic osteolysis activity that, however, did not result in significantly enlarged osteocyte lacunae. In conclusion, we show a recovery of bone microarchitecture and turnover after reversal of hyperthyroidism to a euthyroid state. In contrast, osteocytic osteolysis was initiated in hyperthyroidism, but its effects were not reversed after 4 weeks of weaning. Due to the vast number of osteocytes in bone, we speculate that even minor individual cell functions might contribute to altered bone quality and mineral homeostasis in the setting of hyperthyroidism-induced bone disease. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).