Gross Dental Lesions in the Rat Induced by X-Rays and Neutrons

Castanera, T. J.; Jones, Dave C.; Kimeldorf, Donald J.

doi:10.2307/3571349

Cited by 13 publications

(4 citation statements)

References 7 publications

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“…Some investigators have reported that irradiated teeth decalcify more readily than non-irradiated teeth (Castanera et al, 1963), while others noted no differences in decalcification rates in vitro (Wiemann et al, 1972;Walker, 1975;Shannon et al, 1978a) or even reported decreased enamel and dentin solubility after therapeutic radiation (Joyston-Bechal, 1985;Jansma et al, 1988a;Kielbassa et al, 1999Kielbassa et al, , 2002. Also, it has been shown that ionizing irradiation of dental enamel, at a therapeutic level, has no influence on its permeability and thus on the organic component of enamel (Jansma et al, 1990).…”

Section: Dentitionmentioning

confidence: 99%

Oral Sequelae of Head and Neck Radiotherapy

Vissink

Jansma

Spijkervet

et al. 2003

Critical Reviews in Oral Biology & Medicine

774

512

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In addition to anti-tumor effects, ionizing radiation causes damage in normal tissues located in the radiation portals. Oral complications of radiotherapy in the head and neck region are the result of the deleterious effects of radiation on, e.g., salivary glands, oral mucosa, bone, dentition, masticatory musculature, and temporomandibular joints. The clinical consequences of radiotherapy include mucositis, hyposalivation, taste loss, osteoradionecrosis, radiation caries, and trismus. Mucositis and taste loss are reversible consequences that usually subside early post-irradiation, while hyposalivation is normally irreversible. Furthermore, the risk of developing radiation caries and osteoradionecrosis is a life-long threat. All these consequences form a heavy burden for the patients and have a tremendous impact on their quality of life during and after radiotherapy. In this review, the radiation-induced changes in healthy oral tissues and the resulting clinical consequences are discussed.

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Section: Dentitionmentioning

confidence: 99%

Oral Sequelae of Head and Neck Radiotherapy

Vissink

Jansma

Spijkervet

et al. 2003

Critical Reviews in Oral Biology & Medicine

774

512

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“…A few papers have described proliferative lesions (odontomas or ameloblastomas) of the incisors in rodents as rare spontaneous neoplasms (5,8,22,27) or as hamartomas in inbred (32) or genetically altered (14) rodents. Dental tumors can be induced by treatment with carcinogenic (3,7,9,10) or mitogenic (26) agents, by radiation (6), by dietary imbalances (23,28), and by viruses (12,15). The possibility that chronic dental disease in a significant number of animals may result in stress, unthriftiness, and a general shortening of survival times for animals in chronic toxicology/oncogenicity studies has rarely been considered or addressed.…”

Section: Introductionmentioning

confidence: 99%

Dental Dysplasia in Rats and Mice

Losco¹

1995

Toxicol Pathol

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Malformations of the maxillary incisors, diagnosed as dental dysplasia, were observed as a spontaneous background lesion in 3% (females) to 9% (males) of CD-1® mice and 14.5% (females) to 10.5% (males) of CD@ (Sprague-Dawley) rats in a chronic inhalation study. Lesions were reported grossly as overgrown, maloccluded, or malformed incisors. Microscopic findings included tooth pulp and periodontal abscesses, fractured and necrotic teeth, periodontal cysts, malformations of the incisor roots, and expansile masses, including odontomas, of the incisor roots. Development of lesions followed a pattern of tooth pulp necrosis and/or traumatic disruption of the epithelial root sheath at the base of the tooth. Feeding a powdered ration, which reduced the normal wearing of the incisors, and repeated clipping of overgrown incisors were believed to contribute to the incidence of disease.

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“…The pattern of cell depletion in haemopoietic and spermatogenic tissues is consistent with an immediate cessation of division in stem cells coupled with normal maturation and emigration of existing juvenile cells. The dental lesions in the dehydroheliotridine-treated rats can also be attributed to mitotic inhibition, in this case in the odontogenic epithelium, and are essentially similar to those induced by radiation Castanera, Jones and Kimeldorf, 1963). The period of 5-9 wk elapsing between the administration of dehydroheliotridine and the appearance of the defective zone beyond the gum-line is similar to that observed by Castanera et al in irradiated rats and consistent with the normal growth rate of rat incisors (Schour and Massler, 1942).…”

Section: Discussionmentioning

confidence: 80%