Objective. To assess serum level of Dickkopf-1 in postmenopausal females and its correlation with bone mineral density and serum biochemical markers. Methods. Bone densitometry, serum Dickkopf-1, calcium, phosphorus, and alkaline phosphatase were done in sixty postmenopausal females. Patients were divided according to score into osteoporosis (group I), osteopenia (group II), and normal bone mineral density that served as controls. Results. There was highly significant increase in serum Dickkopf-1 levels in postmenopausal females with abnormal score versus controls ( ). Serum DKK-1 levels correlated negatively with both lumbar score ( , ) and femur score ( , ) and correlated positively with duration of menopause ( , ), while there was no significant correlation between serum levels of either calcium, phosphorus or alkaline phosphatase, and both serum Dickkopf-1 levels and the level of bone mineral density ( ). Conclusion. Postmenopausal females may suffer from osteoporosis as evidenced by bone densitometry. Postmenopausal women with significantly increased serum Dickkopf-1 had more significant osteoporosis. Prolonged duration of menopause and increased serum Dickkopf-1 are important risk factors for the development and severity of osteoporosis. 1. Introduction Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility [1]. It is a chronic progressive disease of multifactorial etiology and one of the most common metabolic bone diseases frequently recognized in postmenopausal women [2]. Osteoporosis is a preventable disease that can result in devastating physical, psychosocial, and economic consequences. Prevention and recognition of osteoporosis are first-line measures to lessen the impact of this condition [3]. Recent evidence suggests that Dickkopf-1 (DKK-1), a soluble inhibitor of the Wnt pathway, may be an active player in several critical aspects of bone biology [4, 5]. The Wnt pathway was first described more than 20 years ago but its role in bone biology was only recently unraveled [6, 7]. The Wnt/β-catenin, also called “canonical” Wnt pathway (1 of the 4 Wnt signaling pathways), is a critical regulator of many aspects of bone and joint physiology [8]. The Wnt/β-catenin pathway stimulates bone formation in several ways: (1) by stimulating osteoblast differentiation and activity and blocking the differentiation of mesenchymal cells toward chondrocytes or adipocytes; (2) by increasing the growth rate of osteoblasts and inhibiting their
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