Estrogen deprivation is a central mechanism in the development of osteoporosis with aging. Results from recent studies also suggest the involvement of estrogens in the pathophysiology of osteoarthritis (OA). Aromatization of androgenic precursors in peripheral tissue is the main source of estrogens in postmenopausal women and in men. However, the importance of aromatase expression in bone is a subject of controversy. This study was undertaken to determine aromatase expression in bone samples from patients with hip fracture and patients with OA.
We studied 104 patients with hip fracture (n = 60) or primary hip OA (n = 44). Aromatase expression was determined in trabecular bone samples from the femoral neck and in osteoblast cultures grown by the primary explant technique (n = 62), using real-time reverse transcriptase-polymerase chain reaction.
Aromatase RNA was detected in bone samples at levels similar to those found in adipose tissue. Transcript levels were significantly lower in bone tissue samples obtained from patients with OA than in those obtained from patients with fracture (P = 0.00001). Likewise, primary cultures of osteoblast cells from OA patients revealed lower aromatase expression than those of cells from fracture patients (P = 0.012). Results were independent of age or sex differences.
Our findings indicate that the aromatase gene is expressed in bone tissue in high amounts, similar to those found in adipose tissue, but transcript levels are lower in tissue samples and osteoblast cultures from patients with OA than in those from patients with hip fracture. Since estrogens may help to prevent local cartilage degradation, it can be speculated that such a reduced expression of aromatase could facilitate the development of OA.