Lead exposure inhibits fracture healing and is associated with increased chondrogenesis, delay in cartilage mineralization, and a decrease in osteoprogenitor frequency.

摘要: Lead exposure continues to be a significant public health problem. In addition acute toxicity, Pb has an extremely long half-life in bone. Individuals with past develop increased blood levels during periods of high bone turnover or resorption. is known affect osteoblasts, osteoclasts, and chondrocytes been associated osteoporosis. However, its effects on skeletal repair have not studied. We exposed C57/B6 mice various concentrations acetate their drinking water achieve environmentally relevant levels, measured by atomic absorption. After for 6 weeks, each mouse underwent closed tibia fracture. Radiographs were followed histologic analysis was performed at 7, 14, 21 days. low concentrations, fracture healing characterized delay bridging cartilage formation, decreased collagen type II X expression 7 days, 5-fold increase formation day 14 delayed maturation calcification, persistence 21. Fibrous nonunions days prevalent receiving very exposures. significantly inhibited ex vivo nodule but had no effect osteoclasts isolated from Pb-exposed animals. No osteoclast number activity observed. conclude that delays doses induces fibrous higher inhibiting the progression endochondral ossification.