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 cons idered to be one of the major hormones regulating postnatal growth. Ho wever, there is dispute as to whether it has a direct or indirect acti on. To study the role of GH we used a polyclonal antiserum to rat GH a nd investigated changes in cell proliferation and enzyme activities as sociated 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 e nzyme activities were quantified in situ microdensitometry. After 1 da y the percentage fo chondrocytes undergoing A synthesis within the pro liferative 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 th e growth plate and that of the proliferative zone. Alkaline phosphatas e (associated with mineralisation) was unchanged but glucose 6-phospha te dehydrogenase activity (associated with cell proliferation) was dec reased. Osteoclastic tartrate-resistant acid phosphatase activity (ass ociated with bone resorption) was also significantly reduced. Similar changes were apparent after 10 days. At no time was the circulating le vel of IGF-I decreased. These data suggest that, during longitudinal g rowth, GH affects the number of proliferating chondrocytes but not the percentage of cells undergoing DNA synthesis, indicating that its pri mary role may be on the commitment of prechondrocytes to a proliferati ve state. Furthermore, while GH does not seem to have any effect on sk eletal mineralisation it may stimulate osteoclastic resorption of the primary spongiosa.