GROWTH-HORMONE AND LONGITUDINAL BONE-GROWTH IN-VIVO - SHORT-TERM EFFECT OF A GROWTH-HORMONE ANTISERUM

The control of longitudinal growth is poorly understood but GH is considered to be one of the major hormones regulating postnatal growth. However, there is dispute as to whether it has a direct or indirect action. To study the role of GH we used a polyclonal antiserum to rat GH and investigated changes in cell proliferation and enzyme activities associated with bone formation and resorption during longitudinal growth. IGF-I levels were measured by two independent RIAs, DNA synthesis by bromo-deoxyuridine incorporated followed by immunocytochemistry and enzyme activities were quantified in situ microdensitometry. After 1 day the percentage fo chondrocytes undergoing A synthesis within the proliferative zone was reduced no other parameters were affected. By day 4 the filling index was the same as in pair-fed animals but the number of chondrocytes synthesising DNA was reduced as the total width of the growth plate and that of the proliferative zone. Alkaline phosphatase (associated with mineralisation) was unchanged but glucose 6-phosphate dehydrogenase activity (associated with cell proliferation) was decreased. Osteoclastic tartrate-resistant acid phosphatase activity (associated with bone resorption) was also significantly reduced. Similar changes were apparent after 10 days. At no time was the circulating level of IGF-I decreased. These data suggest that, during longitudinal growth, GH affects the number of proliferating chondrocytes but not the percentage of cells undergoing DNA synthesis, indicating that its primary role may be on the commitment of prechondrocytes to a proliferative state. Furthermore, while GH does not seem to have any effect on skeletal mineralisation it may stimulate osteoclastic resorption of the primary spongiosa.