Morphometric and Dynamic Studies of Bone Changes in Hypothyroidism

Abstract

Mosekilde, L. & Melsen, F. Morphometric and dynamic studies of bone changes in hypothyroidim. Aota path. microbhl. scand. Sect. A, 86: 56-62, 1978. Born biopsies were performed after tetracycline double-labelling by transfixing the right iliac crest in fourteen hypothymid patients. The bone changes in cortical and trabecular bone were determined by s:mple measurement and point counting on decalcified and undecalcified stained sections and compared to normal controls and to sex and age matched hyperthyroid patients. The amount of trabecular bone and the cortical porosity were unchanged in the hypothyroid patients compared to normal controls, whereas the mean oortical thickness was increased. The amount of osteoid and the length of the oaeoid seams were normal, whereas the mean width of the osteoid seams was decreased. The linear calcification rate in cancellous bone was decreased, as were the active calcification surfaces (tetracycline-labelled) and the percentage of osteoid covered surfaces active in mineralization. The mteoclastic resorption surfaces were unchanged in trabecular bone, whereas the osteoclastl activitty in cortical bone was decreased. The osteocytic outeolysis was normal. The bone changes in hypothyroidism were opposite to the changes in hyperthvroidism charaoterized by a very low bone turn-over w:th a reduced osteoid apposition and bone minerahization rate, an inaotive osteoclastic resorption in trabecular bone and a decreased mteoclastic resorption in captical bone. Mewre hiiumlolagique de la mitsse et de la r6mrption dw travees wseuses. Path. Biol. 12: 23, 24, Castro, J . H., Genuth, S. M., Klein, L.: Comparative response to parathyroid hormone in 1238-1243, 1964.

Optimal bone strength and mineralization requires the type 2 iodothyronine deiodinase in osteoblasts

“…Osteoclast activity and bone resorption surfaces were reduced, and osteoblast activity and osteoid apposition were impaired. The bone formation phase in each remodeling cycle was prolonged 4-fold, resulting in an extended period of secondary mineralization (25)(26)(27). In the current studies, D2KO mice similarly had low bone turnover and impaired osteoblast activity with reduced mineralized surfaces and BFR.…”

“…Studies of the skeletal consequences of hypothyroidism in humans demonstrated low bone turnover and a prolonged bone remodeling cycle with impaired osteoclast and osteoblast function (25)(26)(27). Osteoclast activity and bone resorption surfaces were reduced, and osteoblast activity and osteoid apposition were impaired.…”

“…Thyrotoxicosis increases osteoblast and osteoclast activities, resulting in high bone turnover osteoporosis (2), whereas hypothyroidism results in low bone turnover with reduced osteoblast and osteoclast activities and a net increase in bone mineralization (25)(26)(27). Surprisingly, large population studies demonstrate that both conditions are associated with an increased susceptibility to fracture (3,31,32).…”

Hipervitaminose D em animais

“…Veriϐicou-se que agentes reabsortivos, tais como o PTH, 1,25 (OH) 2 D 3 , TNF-α e as interleucinas, induzem a expressão de RANKL. O T3 induz a expressão de RANKL in vitro, mas esse efeito somente é ampliϐicado quando se adiciona 1,25(OH) 2 D em meio de cultivo com osteoblastos, o que sugere a interação dos hormônios tireoidianos com a vitamina D no mecanismo de reabsorção óssea (Mosekilde et al 1978). A deϐiciência dos hormônios tireoidianos reduz o metabolismo geral e afeta diretamente o recrutamento, a diferenciação, a maturação e o metabolismo das células responsáveis pela aposição, mineralização e reabsorção ós-seas (Burkhart & Jowsey 1967, Jowsey & Detenbeck 1969, Mosekilde et al 1978, Eriksen et al 1986, Banavoc & Koren 2000.…”

“…O T3 induz a expressão de RANKL in vitro, mas esse efeito somente é ampliϐicado quando se adiciona 1,25(OH) 2 D em meio de cultivo com osteoblastos, o que sugere a interação dos hormônios tireoidianos com a vitamina D no mecanismo de reabsorção óssea (Mosekilde et al 1978). A deϐiciência dos hormônios tireoidianos reduz o metabolismo geral e afeta diretamente o recrutamento, a diferenciação, a maturação e o metabolismo das células responsáveis pela aposição, mineralização e reabsorção ós-seas (Burkhart & Jowsey 1967, Jowsey & Detenbeck 1969, Mosekilde et al 1978, Eriksen et al 1986, Banavoc & Koren 2000. A redução da aposição óssea, no hipotireoidismo, se dá por interferência direta (Burkhart & Jowsey 1967), já que T3 e T4 estimulam a expressão de genes nos osteoblastos para a produção de colágeno e osteocalcina (Ross 1996, Varga et al 1997.…”