Abstract

Young rats were x irradiated over the head region with single doses of 1000, 2000, and 3000 r, and other rats received single doses of 1725 and 2400 r administered to the molar regions only. The animals were observed over periods ranging from 2 to 58 days after irradiation. In the first group, the rats irradiated with 1000 r displayed a decreased cellularity of the periodontal membrane, degeneration of osteocytes, and suppressed activity of osteoblasts and osteoclasts. Rats which received 2000 and 3000 r all became moribund or died within 8 to 10 days, exhibiting a characteristic erosion of the epithelial lining of the oral cavity. In the second group, two types of periodontal lesions could be distinguished. One was characterized by severe destruction of the periodontium of either the first or the third molar, leaving the other molars relatively unaffected. These lesions were initiated by ulcerations of adjacent parts of the oral mucous membrane. The other type comprised less severe changes originating in the periodontal tissues proper. They consisted of a lack of proliferation of the interdental papilla epithelium, a deficient inflammatory response, clumping of the collagen, and suppression of the functions of the osteoblasts and osteoclasts. Erosion ofmore » the epithelial lining of the oral mucous membrane observed in the 2000 and 3000 r groups is comparable to the loss of epithelial lining of the intestine of animals given total-body irradiation, and succumbing to intestinal radiation death. The loss of oral epithelium may be an important factor in the syndrome leading to oral radiation death, a previously described syndrome. It was significant that when serious periodontal lesions did develop, they were always seen in connection with ulcerations of mucous membrane areas closely related to, but not part of the periodontal tissues. It was also characteristic that the periodontal tissues ciosest to the mucous membrane lesion were the most affected whereas the remainder were conspicuously unaffected. Severe periodontal lesions were not observed in rats which did not display lesions of the adjacent mucous membrane. Consequently, the severe periodontal destructions observed in some rats did not originate as lesions of the periodontium, but were secondary to ulcerations of the adjacent mucous membrane. The infectious processes thus established expanded relatively unopposed in the radiation-damaged tissue. This mode of development of the severe periodontal lesions is in contrast to observations made on monkeys and dogs, in which the destruction of the periodontium was initiated in the gingiva. In all species, loss or loosening of teeth, caused by inflammatory changes superimposed on decreased resistance to infection, leads to destruction of collagen fibers and resorption of alveolar bone. When rats were subjected to extraction of a molar, this resulted in the development of radioosteomyelitis in some irradiated animals. This condition was characterized by a penetrating destruction of the jaw of an infectious nature with extensive soft and hard tissue necrosis associated with resorption and sequestration of bone. It was considered to be an extension of an inflammatory necrotizing process initiated by ulcerations of mucous membrane areas adjacent to, but not part of the periodontium. (BBB)« less

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