Hormonal effects on the morphology of bone defect healing

Standard defects were produced in the radii of hypophysectomized immature rats. All animals were injected with Methimazole, and grouped according to hormone supplementation, growth hormone (GH), thyroxine (T4), the combination, or no hormones. Lack of GH and T4 caused a retardation of defect healing and callus formation but not a total cessation. The presence of GH in the hypophysectomized animal caused a larger callus due to greatly increased chondrogenesis throughout the 6 week study. Thyroxine in the hypophysectomized animal increased bone metabolism and caused more cartilage and bone formation than seen in the hormone deficient group, but not as great as that seen in the GH injected animals or the T4 and GH injected animals. Growth hormone allowed greater chondrogenesis; T4 enhanced maturation to bone. The combination allowed the development of a callus similar in stage and proportion of tissue to that observed in the pituitary intact animals. The influences of GH and T4 on the healing of a bone defect in the immature rat correspond to influences of GH and T4 on growing epiphyseal plate.