## 1 Introduction  
Sigoren's syndrome (SS) is a chronic autoimmune disease affecting exocrine glands such as the salivary and lacrimal glands. Although it can trigger systemic manifestations, its typical feature is a local predominance of symptoms limited to the salivary and lacrimal glands. SS is termed primary SS (pSS) if it occurs alone, and is not associated with other diseases or secondary SS (sSS) if it occurs in association with autoimmune connective tissue disorders such as rheumatoid arthritis, lupus erythematosus, and systemic sclerosis. Secondary SS coexists less frequently with multiple sclerosis and autoimmune hepatitis [1; 2; 3; 4]. The term \"secondary\" does not refer to a chronological sequence of disease manifestations. Underlying connective tissue diseases may initially present with sica symptoms and only later reveal themselves over the course of the disease. Therefore, differentiation between pSS and sSS is challenging in patients with overlapping disease entities [4]. One of the most common clinical complaints of SS patients is xerostomia and xerophthalmia. Both xerostomia and xerophthalmia result from decreased salivation and lacrimation [1; 2]. However, xerostomia is a clinically broader and more comprehensive concept because it refers to the negative effects of decreased salivation and is usually chronic and persistent [5; 6]. Xerostomia and hyposulavation are often treated as synonyms. However, xerostomia describes a more subjective experience of oral dryness. In turn, hyposulavation refers to objective confirmation of oral dryness [7]. Previous studies reported that at 50% of normal salivary function, even healthy individuals can experience xerostomia [7; 8]. Xerostomia may also occur without a reduction in salivary flow resulting from a change in saliva composition. Therefore, xerostomia may or may not be associated with salivary gland hypofunction. Sometimes, xerostomic complaints can be poor predictors of objective measures of salivary flow [7; 8]. In the study conducted by [PERSON] et al., older adults including diabetic patients and healthy subjects with the lowest parotid saliva flow rates did not have more subjective xerostomic complaints than subjects with normal flow rates [8]. Their findings prove that reported oral dryness depends on an individual's sensitivity to changes in salivation, blood and nerve supply of salivary glands, and their inability to detect xerostomia and distribution of receptors in oral mucosa. Therefore, patients who cannot detect salivary hypofunction could be even more vulnerable to the adverse oral and systemic effects of diminished salivary flow. Oral dryness results from insufficient salivation or a complete lack of saliva. One of the most common examples of salivary gland malfunction resulting in xerostomia is hyposalivation induced by radiotherapy to the head and neck [5]. Radiotherapy to the head and neck irreversibly damages the glandular tissue of the salivary glands. Contrary to xerostomia induced by radiotherapy to the head and neck, some patients experience a subjective impression of oral dryness despite the normal secretory function of the salivary glands. Differences in xerostomia perception may result from various sources of dry mouth and other unidentified mechanisms of adaptation to dryness. Xerostomia may be observed in patients with autoimmune diseases. Possible consequences of impaired saliva secretion include dysphagia, decreased lubricative function of saliva, higher susceptibility to bacterial, fungal, and viral infections, mechanical irritations, and increased periodontitis. The lack of lubricative and protective salivary properties may lead to the development of oral mucosal lesions, including non-specific ulceration, cheilitis angularis, recurrent aphthous stomatitis, denture stomatitis, simple and exfoliative cheilitis, and aphthae [9; 10]. Reduced saliva secretion is associated with a decreased amount of antibacterial, antiviral, and antifungal salivary proteins including histamine, defensins, cystatins, and mucins.