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Pathology - Sjogren's Syndrome
Sjögren’s syndrome is an autoimmune illness that mostly affects the salivary glands. The primary oral complaint is xerostomia (dry mouth), which can lead to difficulties swallowing, dental caries, and inability to speak continuously. Patients with ocular involvement will commonly complain of a gritty sensation beneath the eyelids, likely from damage of bulbar or corneal conjunctival epithelium due to decreased lacrimation from xerophthalmia (dry eye). The physical findings in this patient are typical, including parotid enlargement. Other possible symptoms include weariness, low-grade fever, myalgias, arthralgias, and Raynaud’s phenomenon. The pathophysiology is a result of exocrine (e.g., salivary, lacrimal) gland invasion by T- and B-cell lymphocytes and B-lymphocyte hyperactivity.
Through a number of biological cascades, T-cells trigger glandular epithelial cell death. Ductal and acinar epithelial cells sustain the continuing immunological reaction by improperly generating proinflammatory cytokines and lymphoattractant chemokines. Patient will often have non–organ-specific autoantibodies including ANA and rheumatoid factor (RF); nevertheless, the presence of anti-Ro/SS-A and anti-La/SS-B autoantibodies is specific for Sjögren’s syndrome.
Treatment is mainly supportive; punctal plugs can be used to minimize tear drainage into the nasolacrimal duct, and regular dental care should be established.
Sjögren’s syndrome is an autoimmune illness that mostly affects the salivary glands. The primary oral complaint is xerostomia (dry mouth), which can lead to difficulties swallowing, dental caries, and inability to speak continuously. Patients with ocular involvement will commonly complain of a gritty sensation beneath the eyelids, likely from damage of bulbar or corneal conjunctival epithelium due to decreased lacrimation from xerophthalmia (dry eye). The physical findings in this patient are typical, including parotid enlargement. Other possible symptoms include weariness, low-grade fever, myalgias, arthralgias, and Raynaud’s phenomenon. The pathophysiology is a result of exocrine (e.g., salivary, lacrimal) gland invasion by T- and B-cell lymphocytes and B-lymphocyte hyperactivity.
Through a number of biological cascades, T-cells trigger glandular epithelial cell death. Ductal and acinar epithelial cells sustain the continuing immunological reaction by improperly generating proinflammatory cytokines and lymphoattractant chemokines. Patient will often have non–organ-specific autoantibodies including ANA and rheumatoid factor (RF); nevertheless, the presence of anti-Ro/SS-A and anti-La/SS-B autoantibodies is specific for Sjögren’s syndrome.
Treatment is mainly supportive; punctal plugs can be used to minimize tear drainage into the nasolacrimal duct, and regular dental care should be established.
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