Abstract

There has been a paradigm shift in the understanding of the pathogenesis of sialoliths, also known as salivary calculi, as a result of clinicopathologic and experimental investigations that revealed that sialolithiasis is secondary to chronic sialadenitis. Clinical and histologic features were statistically analyzed in cases of chronic submandibular sialadenitis and revealed that there is a chronological progression of increasingly severe chronic sialadenitis with, in many cases, the eventual development of a sialolith. Postmortem and electronmicroscopic investigations revealed that microscopical concretions called sialomicroliths are present in all normal submandibular glands and a minority of normal parotids, and in all cases of chronic submandibular sialadenitis. However, sialomicroliths do not develop into sialoliths, and experimental investigations added the missing pathogenic link. Parasympathectomy of the submandibular gland of cat caused a greatly increased occurrence of sialomicroliths, which led to the realization that a lack of secretory activity causes sialomicroliths. The present understanding of the pathogenesis of sialoliths is as follows: secretory inactivity leads to an accumulation of sialomicroliths and allows ascent of the main duct by commensal microbes; impaction of sialomicroliths in small intraglandular ducts produces obstructive atrophic foci, in which the microbes can proliferate and cause inflammatory swelling, which is obstructive and may eventually involve the entire gland; partial obstruction of a large duct allows calcification of stagnant secretory material, which is rich in calcium, to accrete and become a sialolith. Any form of chronic sialadenitis or partial obstruction may eventually lead to the development of a sialolith.

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