Title

Etidronate inhibits the thyroid hormone-induced bone loss in rats assessed by bone mineral density and messenger ribonucleic acid markers of osteoblast and osteoclast function

UMMS Affiliation

Division of Endocrinology; Department of Cell Biology

Date

12-1-1993

Document Type

Article

Subjects

Animals; Biological Markers; Bone Density; Etidronic Acid; Femur; Male; Osteoblasts; Osteoclasts; Osteoporosis; RNA, Messenger; RNA, Ribosomal, 28S; Rats; Spine; Thyroxine

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

TSH-suppressive doses of thyroid hormone are associated with bone loss. We have previously reported that L-T4 decreases femoral, but not vertebral bone mineral density (BMD) in rats. As bisphosphonates are able to decrease bone resorption, especially in high bone turnover states, we investigated the potential effects of etidronate disodium (EHDP) on L-T4-induced bone loss in the rat model by assessing BMD and gene expression of osteoblast (osteocalcin, osteopontin, type I collagen, and alkaline phosphatase), osteoclast (tartrate-resistant acid phosphatase), and cell growth (histone) markers in the skeleton. L-T4 administered for 20 days decreased BMD in the femur, but had no effect on the lumbar spine. EHDP alone had no effect on femoral or vertebral BMD, but did prevent the L-T4-induced bone loss in the femur. L-T4 increased mRNA levels of alkaline phosphatase, tartrate-resistant acid phosphatase, and histone H4 in the femur, but not in the vertebrae. EHDP, which alone had no effect on gene expression in the femur or vertebrae, inhibited the effect of L-T4 on mRNA markers in the femur. The results demonstrate that EHDP can prevent the L-T4-induced decrease in femoral BMD in rats that is associated with the prevention of changes in mRNA markers of osteoclast and osteoblast function. EHDP and other bisphosphonate compounds may be useful in the prevention of thyroid hormone-induced bone loss in humans.

Rights and Permissions

Citation: Endocrinology. 1993 Dec;133(6):2502-7.

Related Resources

Link to Article in PubMed

Journal Title

Endocrinology

PubMed ID

8243271