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

Environmental Health Perspectives

Volumn 113, Issue 6, 2005, Pages 749-755

  Carmouche, Jonathan J ^a   Puzas, J Edward ^a   Zhang, Xinping ^a   Tiyapatanaputi, Prarop ^a   Cory Slechta, Deborah A ^b   Gelein, Robert ^b   Zuscik, Michael ^a   Rosier, Randy N ^a   Boyce, Brendan F ^a   O'Keefe, Regis J ^a   Schwarz, Edward M ^a  

^a UNIVERSITY OF ROCHESTER MEDICAL CENTER   (United States)

^b UNIVERSITY OF ROCHESTER SCHOOL OF MEDICINE AND DENTISTRY   (United States)

Author keywords

Endochondral ossification; Fracture healing; Lead; Osteoblast; Osteoclast; Pb; Pb toxicity

Indexed keywords

DRINKING WATER; LEAD ACETATE;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; ATOMIC ABSORPTION; BONE MATURATION; BONE MINERALIZATION; BONE RADIOGRAPHY; CALCIFICATION; CARTILAGE CELL; CELL ACTIVITY; CELL ISOLATION; CHONDROGENESIS; CONTROLLED STUDY; ENCHONDRAL OSSIFICATION; ENVIRONMENTAL EXPOSURE; EX VIVO STUDY; FRACTURE HEALING; FRACTURE NONUNION; HISTOLOGY; LEAD BLOOD LEVEL; MOUSE; MOUSE STRAIN; NONHUMAN; OSTEOBLAST; OSTEOCLAST; PRIORITY JOURNAL; TIBIA FRACTURE;

ANIMALS; CARTILAGE; CELL COUNT; CELLS, CULTURED; CHONDROGENESIS; FEMALE; FRACTURE HEALING; LEAD; MICE; MICE, INBRED C57BL; OSTEOCLASTS; TIBIA;

ANIMALIA;

EID: 20844463259     PISSN: 00916765     EISSN: None     Source Type: Journal    
DOI: 10.1289/ehp.7596     Document Type: Article

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