Abstract

Summary A retrospective study of 107 patients * with chronic recurrent parotitis and a prospective study of 25 patients with chronic recurrent parotitis and 6 patients with Sjogren's syndrome have been carried out. In most of the patients with chronic recurrent parotitis the main parotid duct is more tortuous and bent under a more acute angle while the ducts of the first and second order form a more obtuse angle than normal. Consequently, the secretion of saliva becomes rather difficult and its flow rate is diminished. In 25 subjects with chronic recurrent parotitis biopsy has been performed and the dominant histological finding was infiltration of the interstitium, while histochemically, mucin has been found both in ducts and acini in 72% of the cases. The parotid glands of subjects from the control group secreted more saliva than the unaffected glands of patients with unilateral parotitis. In the cases of unilateral parotitis the levels of IgA and IgG in the saliva of the affected glands have been statistically significantly higher compared to saliva of the unaffected glands in the same patients. In the course of remission of the disease the level of immunoglobulins in saliva from the affected glands has been decreased. The levels of IgA and IgG of parotid saliva in subjects from the control group have been markedly higher compared to the level of parotid saliva of the unaffected glands in patients with unilateral parotitis. After injecting antigens into the parotid duct the levels of IgA and IgG in saliva of the control group have been significantly increased. We have come to the conclusion that in the aetiopathogenesis of chronic recurrent parotitis the main factors which cause and maintain infection are diminished salivation, the diminished immunological capacity of saliva as well as the histological and anatomo-topographical characteristics of the parotid gland. The pathophysiology of the disease can be summarized as follows: Diminished secretion of the immunologically poor-quality saliva and its reduced flow rate have as their sequelae inadequate selfcleansing and retrograde spread of microorganisms from the mouth into the gland. The infection leads to partial metaplasia of serous cells into mucous cells. — Mucus flows with difficulty through narrow serous ducts and mucous plugs are formed. — Accumulation of saliva, infiltration and swelling of tissue produce inactivity and pressure atrophy of the gland. — Proteolytic ferments lacking alpha 1 antitrypsin lead to the destruction of parenchyma and its replacement by connective and fatty tissue. — Obstruction of ducts by mucous plugs and proliferated tissue leads to still greater retention of salivation, dilatation and sacculation of small ducts and acini which result in further decrease in secretion of saliva and its antibacterial agents. All these favour the invasion by bacteria and thus the establishment of a vicious circle.

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