Abstract

Although acinar atrophy occurs frequently in salivary diseases, the relationship between structural changes and functional decrements is not well-established, and the potential for recovery of histological and functional integrity has not been wholly quantified. We aimed, therefore, to develop further our understanding of pathological acinar atrophy. Stensen's duct was ligated for periods up to six weeks and, in separate experiments, was de-ligated after two weeks and allowed to recover for up to two weeks. Qualitative and quantitative histological analyses were carried out. Additionally, the ability of enzymatically dispersed cells from ligated and de-ligated glands to respond to neurohormonal stimuli was also measured. The results confirmed that totally obstructed glands undergo a rapid, progressive severe atrophy amounting to absolute losses of over 85% of acinar tissue by two weeks. Acinar shrinkage and cell losses through apoptosis accounted for the glandular atrophy. Remaining intralobular epithelia consisted of extremely atrophic acini and numerous duct-like structures with intermediate forms. Dispersed cells from atrophic glands exhibited agonist-induced release of chloride similar to normal. Together, these structural-functional results confirm the persistent viability of acinar-like cells in the obstructed gland and suggest that the duct-like structures are derived from surviving atrophic acini. De-ligated glands exhibited a near-normal recovery of structure by two weeks. Their enzymatically dispersed cells responded normally to agonist stimulation. The results support the view that pathological atrophy is largely similar to physiological atrophy, providing a mechanism for acinar cell survival under adverse conditions, with the possibility of eventual recovery.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call