Chronic Submandibular Sialadenitis: Ultrastructure and Phosphatase Histochemistry

Abstract

Eleven specimens of chronic submandibular sialadenitis were examined. A reduction in secretory material in acinar cells was seen with increasing atrophy until the acini resembled intercalary ducts. Myoepithelial cells and basement membrane were sometimes more conspicuous. Striated ducts showed a reduction of the folding of the plasma membranes in the basal part, and striated and excretory ducts showed a reduction in mitochondria. This possibly represents a functional atrophy secondary to reduced salivary flow. Very atrophic parenchyma largely consisted of simple cells. Phagosomes and apoptotic bodies were occasionally seen, and appear to be involved in the atrophy. Thiamine pyrophosphatase in the Golgi apparatus and acid phosphatase in the GERL were demonstrated in moderately atrophic parenchyma. This is similar to normal and indicates continuing synthetic activity. Acid phosphatase was demonstrated in lysosomes, which appear to be involved in the atrophy by their role in phagy. Alkaline phosphatase was occasionally demonstrated at luminal surfaces, and is likely to be involved in resorption of obstructed luminal contents. The changes are similar to those seen in experimentally obstructed glands and indicate that much of the parenchyma survives by adaptation to the altered environment which forms the basis for the successful results following conservative therapy.

Biological behavior of myoepithelial cells in the regeneration of rat atrophied sublingual glands following release from duct ligation

“…However, the remaining ducts and immature acini were commonly In this study, myoepithelial cells often displayed bizarre appearances with protrusion of cell processes into interstitial spaces and irregular folds of basal lamina. A similar appearance of myoepithelial cells has previously been reported in the experimental atrophy of 15 other salivary glands (Emmelin et al 1974, Garrett & Emmelin 1979, Takahashi et al 2001, in human sialadenitis (Harrison & Badir 1998), and in the involution of mammary glands (Radnor 1972, Walker et al 1989 with their differentiation and maturation, since the bizarre appearances were caused by atrophy and loss of underlying cells (Garrett & Emmelin 1979). And the biological significance of the bizarre shape of myoepithelial cells in the atrophy may be to contribute to the rapid recovery in accordance with underlying cell maturation.…”

Morphological and functional changes of the rat parotid glandular cells by clipping and reopening the parotid duct, using HAM8 antibody

“…This has been demonstrated using both TUNEL and TEM (Takahashi et al ., 2004). Acinar cells are also removed by apoptosis in regressive conditions such as experimental atrophy, chronic sialadenitis and Sjögren syndrome (Walker & Gobe, 1987; Harrison & Badir, 1998; Scott et al ., 1999; Takahashi et al ., 2001, 2002). However, the salivary gland regenerates after reopening of the duct.…”

A morphogenetic concept of salivary duct regeneration and metaplasia

“…In contrast to conventional squamous cell MP developing in striated/excretory ducts, the lack of additional gain of CK 13 and CK 10 in necrotizing sialo-MP presumably is due to a more restricted morphogenetic capacity in the differentiated and Bcl-2-negative acinar and intercalated duct cells. Despite the documented proliferative capacity of myoepithelial cells in the regular duct and especially in chronic sialadenitis or ductal blockage, myoepithelial cells are involved neither in necrotizing sialo-MP nor in any other form of MP [16,29].…”