TY - JOUR
T1 - Rationale for active vitamin D analog therapy in senile osteoporosis
AU - Åkesson, K.
AU - Lau, K. H.W.
AU - Baylink, D. J.
N1 - doi: 10.1007/s002239900195. 1 Departments of Medicine and Biochemistry, Loma Linda University and Mineral Metabolism, Jerry L. Pettis Memorial V.A. Medical Center, 11201 Benton Street, Loma Linda, California, 92357, U.S.A. Show details doi: 10.1007/s002239900195. 1 Departments of Medicine and Biochemistry, Loma Linda University and Mineral Metabolism, Jerry L. Pettis Memorial V.A.
PY - 1997/1
Y1 - 1997/1
N2 - Osteoporosis is diagnosed when bone density decreases below the fracture threshold, a change that is associated with decreased biomechanical integrity and fracture. There are two types of primary osteoporosis: postmenopausal osteoporosis and senile osteoporosis. Postmenopausal osteoporosis is due to some combinations of a low peak bone density and a high rate of bone loss during the early postmenopausal years. The bone loss is primarily due to estrogen deficiency, which leads to increases in resorbing cytokines and a consequent increase in bone resorption. The pathogenesis of senile osteoporosis is less well understood and includes factors in addition to estrogen deficiency. A potential etiological factor is the vitamin D deficiency that occurs with advancing age. Severe vitamin D deficiency in the adult leads to osteomalacia, whereas a mild deficiency, which is common in the elderly, is rarely associated with mineralization defects but instead could lead to development of secondary hyperparathyroidism and osteoporosis. There are basically two types of vitamin D deficiency: (1) primary vitamin D deficiency which is due to a deficiency of vitamin D, the parent compound of the active metabolite 1,25(OH)2D3; and (2) a deficiency of 1,25(OH)2D3 action resulting from either decreased production of 1,25(OH)2D3 by the kidney or from decreased responsiveness to 1,25(OH)2D3 of target tissues, i.e., resistance. Both types of deficiencies could occur with aging, and both have been implicated as potential causes of senile osteoporosis. In this paper, we would like to advance the hypothesis that the age-related deficiency in 1,25(OH)2D3 action plays a role in the pathogenesis of senile osteoporosis. We will provide evidence to support the concept that a deficiency of 1,25(OH)2D3 action exists in the elderly, which plays a role in age-related bone loss, and that this deficiency of 1,25(OH)2D3 action can be successfully treated with 1,25(OH)2D3 or 1α-hydroxy vitamin D3 [1α(OH)D3].
AB - Osteoporosis is diagnosed when bone density decreases below the fracture threshold, a change that is associated with decreased biomechanical integrity and fracture. There are two types of primary osteoporosis: postmenopausal osteoporosis and senile osteoporosis. Postmenopausal osteoporosis is due to some combinations of a low peak bone density and a high rate of bone loss during the early postmenopausal years. The bone loss is primarily due to estrogen deficiency, which leads to increases in resorbing cytokines and a consequent increase in bone resorption. The pathogenesis of senile osteoporosis is less well understood and includes factors in addition to estrogen deficiency. A potential etiological factor is the vitamin D deficiency that occurs with advancing age. Severe vitamin D deficiency in the adult leads to osteomalacia, whereas a mild deficiency, which is common in the elderly, is rarely associated with mineralization defects but instead could lead to development of secondary hyperparathyroidism and osteoporosis. There are basically two types of vitamin D deficiency: (1) primary vitamin D deficiency which is due to a deficiency of vitamin D, the parent compound of the active metabolite 1,25(OH)2D3; and (2) a deficiency of 1,25(OH)2D3 action resulting from either decreased production of 1,25(OH)2D3 by the kidney or from decreased responsiveness to 1,25(OH)2D3 of target tissues, i.e., resistance. Both types of deficiencies could occur with aging, and both have been implicated as potential causes of senile osteoporosis. In this paper, we would like to advance the hypothesis that the age-related deficiency in 1,25(OH)2D3 action plays a role in the pathogenesis of senile osteoporosis. We will provide evidence to support the concept that a deficiency of 1,25(OH)2D3 action exists in the elderly, which plays a role in age-related bone loss, and that this deficiency of 1,25(OH)2D3 action can be successfully treated with 1,25(OH)2D3 or 1α-hydroxy vitamin D3 [1α(OH)D3].
UR - https://www.scopus.com/pages/publications/0031023174
UR - https://www.scopus.com/pages/publications/0031023174#tab=citedBy
U2 - 10.1007/s002239900195
DO - 10.1007/s002239900195
M3 - Article
C2 - 9030489
SN - 0171-967X
VL - 60
SP - 100
EP - 105
JO - Calcified Tissue International
JF - Calcified Tissue International
IS - 1
ER -