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Biomedical subjects

K L Burgess

Publications and source records attributed to K L Burgess.

At least 19 recordsLinked to original sources
PubMed1998

Cell population changes during atrophy and regeneration of rat parotid gland.

Limited data exist regarding the changes in number and location of myoepithelial cells during salivary gland atrophy and regeneration. Through the use of double immunohistochemical labeling for muscle-specific actin and amylase coupled with morphometric analysis, this study investigated the changes in distribution and proportion of cell types during salivary gland atrophy/regeneration phases in a model previously used to study proliferation in rat parotid gland. The double immunohistochemical labeling clearly showed the changes in proportion of cell types in the atrophying and regenerating glands. The morphometric analysis showed that the relative myoepithelial area increased (as did the intercalated duct and striated duct areas) as the gland atrophied. Myoepithelial cells occupied 19.0% of the total epithelial area by day 7 of atrophy, up from 2.7% in the resting gland. Regeneration of acinar cells was obvious 1 day after duct release. The myoepithelial cell area decreased to 4.3% of the total epithelial area by day 14 of regeneration; this value was higher than the percentage of area in the resting gland (p = 0.02). The relative areas of acinar, striated duct, and intercalated duct cells returned to resting levels after 14 days of regeneration. The morphometric and histologic results of this study show that the parotid gland is capable of regenerating to essentially normal anatomic condition after 7 days of gland atrophy and then 14 days of regeneration. Each type of cell, however, responded to the atrophy and regeneration differently. Atrophy of salivary glands from radiation therapy. Sjögren's syndrome, or sialadenitis is an important clinical problem. Study of the salivary gland response to atrophy and regeneration may provide a framework for designing strategies for the radioprotection of salivary glands or methods by which to treat or reverse the effects of gland atrophy.

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PubMed1996

Myoepithelial cells actively proliferate during atrophy of rat parotid gland.

Despite limited supporting evidence, salivary gland myoepithelial cells are said to be differentiated cells with little or no capacity to replicate; they presumably develop from stem cells. This study investigated the proliferative potential of myoepithelial cells with an antibody to proliferating cell nuclear antigen and a rat model. This model involved clamping of the parotid duct causing atrophy of the gland and then releasing the duct followed by gland regeneration. Rats were sacrificed at time points during atrophy and regeneration phases and the number and location of cycling myoepithelial cells assessed. Cycling myoepithelial cells were identified with double immunohistochemical staining, cycling cells with proliferating cell nuclear antigen-positive nuclei within muscle-specific actin-positive cytoplasm (the latter identified with antibody HHF35). The results show that baseline proliferative rates of myoepithelial cells in both the resting and fully regenerated gland ranged from 0.3% to 2%, similar to rates for other major cell types in the normal rat gland. A peak myoepithelial cell proliferative rate of 23% occurred at day 5 during the atrophy phase. Rates during the regenerative phase were not significantly different than the baseline levels. Similarities of rat and human parotid gland and the definite proliferative capacity of myoepithelial cells indicates that these specialized cells must be considered one of the potential progenitor cells for human salivary gland tumors.

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