Histopathological studies of the tarsal (Meibomian) glands in experimental PCB poisoning in rhesus monkeys

15 rhesus monkeys (Macaca mulatta) were used for making the experimental models of oral polychlorinated biphenyls (PCB) poisoning. At autopsy the eyelids of these animals were obtained for histopathological studies of the tarsal (Meibomian) glands in PCB poisoning. In the early stage of the process the stratified squamous epithelial cells of the ducts of the tarsal glands manifested hyperkeratosis, hyperplasia and dilated lumen. The acini had no significant changes in this stage. Thereafter, when keratinized materials accumulated in part of the ducts, the acini surrounding the ducts began to atrophy and the lipid-forming cells of the acini disappeared as they were shed and were replaced by squamous epithelial cells (squamous metaplasia). In the next stage, these changes of the ducts and the acini extended to the whole area of each tarsal gland. In the last stage, when cystic formation of the tarsal glands was complete, the epithelium of its wall became thin and the acini had disappeared. Hypersecretion of the tarsal glands, one of the main ocular signs of PCB poisoning patients, has been described. Histopathologically, however, the ducts of the tarsal glands were filled with accumulated keratin and the acini became atrophic or disappeared. Therefore, it was clear that the secretion of the tarsal glands was deteriorated rather than enhanced. Squamous metaplasia of the acini of the tarsal glands in PCB poisoning was more prominent than that of the other sebaceous glands. This pathological finding has not been observed in cysts of the tarsal glands (Meibomian cyst) caused by obstruction of the ducts. It remained uncertain whether the squamous metaplasia was characteristic of the tarsal glands in PCB poisoning.