All members of a weimaraner litter had clinical and radiographic signs of hypertrophic osteodystrophy shortly after weaning. Three dogs were necropsied. Radiographic metaphyseal densities, which are used to make a clinical diagnosis of hypertrophic osteodystrophy, were found to result from elongation of the calcified cartilage lattice of the primary spongiosa. Intertrabecular acute inflammation was associated with necrosis, failure to deposit osseous tissue on the calcified-cartilage lattice, and trabecular microfractures. This process led to metaphyseal infraction and separation of the epiphysis. Defective bone formation (osteodystrophy) was considered a secondary process resulting from inflammation of osteochondral complexes, marrow, and periosteum. Enamel hypoplasia also was found to be associated with inflammation of the dental crypt, and abnormal enamel matrix was observed in the developing teeth. The histopathology of the bones and teeth was different from alterations which occur in infantile scurvy or congenital syphilis, although these diseases of man have radiographic similarities to canine hypertrophic osteodystrophy. Because the radiologic lesion is nonspecific, a clinical diagnosis of hypertrophic osteodystrophy is not necessarily diagnostic of a specific disease due to a single etiologic agent. Liver levels of ascorbic acid were within the normal range. Although an infectious agent could not be identified, the conditions may have an infectious origin with systemic manifestations.