Regarding the Lack of Evidence for a Microbial Etiology of Sialolithiasis

There was a paradigm shift in the understanding of the etiology and pathogenesis of sialolithiasis as a result of extensive experimental and clinicopathological investigations at the turn of the century, which have continued to this day. Essentially, sialoliths were found to be secondary to obstructive sialadenitis usually caused by sialomicroliths associated with a lack of secretory activity, when secretory granules degenerate or when stagnant saliva, both rich in calcium, allow ionic calcium to precipitate onto exposed phospholipid of damaged membranes. A recent article by Kao et al. published in The Laryngoscope refers to this work but seriously misrepresents it. The article states: “Harrison induced sialolith formation in rats and cats that were given repeated doses of isoprenaline and high calcium supplementation (p 3).”However, this only applied to the experiments involving rats. The critical experiments involving cats found that secretory inactivity caused by parasympathectomy led to an increased formation of sialomicroliths. The article further states that patients with sialolithiasis “typically have normal calcium levels and no preceding sialadenitis (p 4).” However, a clinicopathological investigation of 154 cases of chronic submandibular sialadenitis found that sialoliths were only present in 93 out of 136 specimens for which data was available, and sialoliths were more frequent with increasing duration of symptoms, indicating that they were secondary to the sialadenitis. Also, Capaccio et al. found 54 patients with chronic sialadenitis but no evidence of sialoliths or other clinically detectable obstruction out of a total of 263 patients. Furthermore, the levels of calcium in the salivary glands are high, and calcium is released when secretory granules disintegrate during secretory inactivity to precipitate on exposed phospholipid of damaged membranes or to stagnate in lumina and precipitate there on exposed phospholipid. Kao et al. examined one sialolith that was sectioned and viewed lightmicroscopically, and stated, “The core region of the sialolith was imaged (p 2).” However, this ignores the extensive investigations using computed microtomography and electronmicroscopy by Nolasco et al., which showed that the core of a sialolith was often not at the center and could not be reliably found by conventional microscopy. Thus, what Kao et al. assumed to be a core wasmost likely part of the sialolith formed subsequent to the core, which would be expected to containmicrobes. The micrographs in Kao et al. lack analytical evidence of calcium, and interpretation of them is no more than a speculative assumption. The proposal that immune cells interact with biofilm and calcium nanoparticles to initiate sialolith formation is clearly not substantiated.