Kimura's Disease

Most cystic lesions of the major salivary gland are cystic neoplasms. Benign cysts are epithelial lined cavities usually containing fluid or semisolid material, incidence is 2-5%. Benign cysts of the salivary gland are classified into three types:
a) Lymphoepithelial cysts
b) Salivary duct cysts
c) Dysgenetic cysts[28]
a) Lymphoepithelial cyst
Bernier and Bhaskar introduced the term lymphoepithelial cysts to stress that it is not an embryologic remnant. Lymphoepithelial cysts are considered distinct entities from the lymphoepithelial lesions.[29] Usually there is a well circumscribed, asymptomatic mass in the superficial portion of the gland. They range from 0.5-6.0 cms and an average of 2.5 cms, M: F 2.7: 1.0, age at presentation is 18-79

According to Kung et al. Kimura’s disease was first described in China in 1937. This entity became known as Kimura’s disease, after Kimura et al. reported a similar case in 1948. It is a chronic inflammatory condition of unknown cause. The disease occurs predominantly in young and middle aged, median age of onset ranges from 27 to 40 years. Males are more commonly affected than females. Rosai et al. were first to note that Kimura disease is different from angiolymphoid hyperplasia. Kimura’s disease occurred mainly around the ear with frequent involvement of salivary gland.[30] The lesions are rubbery and irregular or nodular. Cut surface is gray to light brown and may contain embedded lymph nodes and attached salivary gland and muscle.[28] Microscopically the lesions are unencapsulated and ill defined, characterized by fibrocollagenous tissue, lymphoid tissue and a mixed inflammatory cell infiltrate with numerous eosinophils. Eosinophilic abscess, polykaryocytes of Warthin- Finkeldy are sometimes present in germinal

Sjogren’s syndrome is a disease of middle aged women with a female to male ratio of 10:1.[12] It is a chronic lymphoproliferative disorders that shows a spectrum of clinical manifestations and presents a primary or secondary disease. It can involve only exocrine glands, in which it is called as glandular, or extend to involve other sites as well, in which case it is called extraglandular.
The exact etiopathogenetic mechanism is unknown. Polyclonal B-cell hyperreactivity with abnormalities of autoregulation have been reported, the histopathologic substrate of Sjogren’s syndrome is characterized by presence of lymphocytic infiltrates in glandular and extraglandular sites. Microscopic examinations of enlarged parotid or submandibular glands reveal benign lymphoepithelial lesion, characterized by epimyoepithelial islands in a lymphocytic infiltrate with replacement of acini. In the minor salivary glands the characteristic feature is focal lymphocytic