Get your own Free Home PageSALIVARY GLAND DISEASES
Sialadenitis - Decreased salivary flow with stasis is a key factor in chronic sialadenitis. Like acute sialadenitis, this condition is more common in the parotid gland. Its development is often associated with a previous episode of acute suppurative inflammation with subsequent glandular destruction. Another possibility is the recurrent parotitis of childhood which has continued into adulthood. With the onset of the chronic inflammatory process, alterations in salivary chemistry and enzyme and immunoglobulin content take place. Sialectasis, ductal ectasia, and acinar atrophy occur, accompanied by a lymphocytic infiltrate. Symptoms include recurrent mildly painful swelling of the parotid which often accompany eating.
Sialolithiasis -The formation of salivary gland calculi occurs in the submandibular gland approximately 80 to 90% of the time and in the parotid gland the remaining 10 to 20%. The sublingual and minor salivary glands are rarely involved. Stone formation is thought to be more common in the submandibular gland secondary to the higher mucin content of its saliva and the anti-gravity flow of saliva within the duct. Its saliva is also more alkaline and has a higher calcium and phosphorous content( that shows as an increased plaque on the teeth ). Submandibular stones are usually also larger in size. Serum calcium and phosphorous levels have no known correlation with the formation of calculi. Calculi may be found within the ductal system itself or within salivary gland parenchyma. In most cases of sialolithiasis, a single calculus is involved. Stone formation occurs via the deposition of calcium phosphate and an organic matrix of carbohydrates and amino acids about a nidus of debris or other material. With the occurrence of ductal obstruction, stasis of saliva may occur with varying degrees of surrounding inflammation and possible ascending bacterial infection. Streptococcus viridans is a common offending pathogen. Stone formation most often occurs in middle-aged males and may result in intermittent salivary gland swelling and discomfort, especially with eating. Calculi have been associated with the existence of chronic sialadenitis and may present as an acute suppurative sialadenitis.
Sjögren's syndrome is associated with inflammation of salivary and tear glands, resulting in dry mouth and eyes.
MILD SIALOADENITIS: A COMMON FINDING IN PATIENTS WITH HEPATITIS C VIRUS INFECTION.
Pirisi M; Scott C; Fabris C; Ferraccioli G; Soardo G; Ricci R;
Toniutto,P; Avellini C; Vitulli D; Miotti AM; et al; Dept. of
Internal Medicine, University of Udine, Italy. Scand J Gastroenterol,
1994 Oct, 29:10, 940-2
BACKGROUND: Sjögren's syndrome (SS) is an autoimmune disease of presumed viral origin; sialoadenitis has been reported to occur in hepatitis C virus (HCV) infection. METHODS: Lip biopsy specimens were graded in 32 consecutive patients with either HCV-related chronic liver disease or SS. RESULTS: Seventeen of 22 HCV-positive patients had sialoadenitis, although generally mild (15 of 17, grades I-II). Severe inflammation (grades III-IV) was observed in 8 of 10 patients with SS (chi-square = 12.6; P < 0.0005). Moreover, HCV-positive patients with sialoadenitis differed from patients with SS in female sex prevalence (6 of 17 versus 10 of 10; chi-square = 10.9; P = 0.0001) and presence of serum antinuclear autoantibodies (0 of 17 versus 9 of 10; chi-square = 23.0; P < 0.0001). Five of 13 HCV-positive patients and 7 of 8 patients with SS were HLA-DR3-positive (chi-square = 4.9; P < 0.05). CONCLUSIONS: Sialoadenitis of HCV-related liver disease is common but differs from SS with regard to predisposing genetic factors, expression of autoimmune markers, and histopathologic severity.
THE INVOLVEMENT OF THE LIVER IN SJÖGREN'S SYNDROME.
Vogel C; Wittenborg A; Reichart P; Oral Surg Oral Med Oral Pathol, 1980 Jul, 50:1, 26-9
Liver involvement in Sjögren's syndrome is little known in oral medicine. The involvement of the oral cavity and salivary glands is often diagnosed as an additional symptom during a general internal examination. This study shows that, even in the case of extensive liver involvement with considerable hepatic enzyme alterations, complaints in the mouth and jaw region can initially lead the patient to seek the advice of a dentist.
THE HEPATITIS B VIRUS AS A PROBABLE ETIOLOGICAL FACTOR IN SJÖGREN'S DISEASE
Aprosin ZG; Serov VV; Lopatkina TN; Ter Arkh, 1993, 65:4, 73-8
Various profiles of serum HBV markers (HbsAg) were identified in 16 patients, markers of active replication in 4 patients (HbeAg, 2 cases; HBcAb IgM, 1 case; HBcAb IgM and HbsAg IgM, 1 case) out of 22 patients with Sjögren disease (SD) having serum HBV markers and systemic manifestations. Of these 3 had a history of acute viral hepatitis, 12 were previously at risk to be infected with hepatitis viruses, 7 had neither the disease nor its risk factors, none of them had chronic active hepatitis or hepatic cirrhosis, 7 exhibited clinical signs of pseudolymphoma, 1 had serum monoclonal IgM kappa in the presence of HBV active replication markers (HBsAg IgM, HbcAb IgM). The present and previous data (on association of SS with chronic active hepatitis and hepatic cirrhosis due to HBV) suggest the involvement of the virus in SD etiology.
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