الفهرس 
AIM OF THE WORKOnly 14 pages are availabe for public view
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Abstract
In the pathogenesis of LP, specifically involving the cellular arm of the immune system. The inflammatory infiltrate consists primarily of T cells and macrophages. Plasma cells are rarely seen and immune deposits are not characteristic. TNF-α is a cytokine produced by a wide variety of cell types, including macrophages, T and B lymphocytes, Langerhans cells, endothelial cells and keratinocytes. This cytokine is involved primarily in T-cell-mediated cytotoxic reactions, and among its diverse biological effects, it inhibits the proliferation and stimulates differentiation of keratinocytes.
The production or release of TNF-α within the LP lesions may play a key regulatory role in the immunological reactions that are involved in the pathogenesis of this disease. TNF-α induce expression of leukocyte- Lichen planus is a relatively common mucocutaneous disease of unknown etiology. Although its cause still is unknown, cell-mediated immune dysfunction is implicated in its pathogenesis. Despite recent advances in understanding the immunopathogenesis of lichen planus the initial triggers of lesion formation and the essential pathogenic pathways are unknown. It is therefore not surprising that the clinical management of LP poses considerable difficulties to the dermatologist.
A large body of evidence supports a role for immune dysregulation binding adhesion molecules on postcapillary venular endothelial cells, which promotes infiltration of the lesion by T lymphocytes and macrophages. Once through the endothelial junctions, the movement of T lymphocytes is directed by gradients of chemotactic agents, of which TNF-α is one of them. The biologic effects of TNF-α on cultured keratinocytes are diverse and include cytotoxicity at high concentrations and inhibition of proliferation at lower concentrations. Recently, the basis of the peculiar Th1 cytokine bias observed in OLP was shown to have a genetic background. Indeed, genetic polymorphism of the first intron of the promoter gene of IFN-γ was shown to be an important risk factor for the development of oral lesions of LP, whereas an increase in the frequency of the – 308A TNF-α allele was demonstrated in patients who displayed LP of the mouth and skin.
The elevated TNF-α serum levels may be associated with the induction and/or perpetuation of the pathogenetic and apoptotic events in the lesional LP epithelium. The present study aimed to evaluate serum level of TNF-α in patients with lichen planus after exclusion of other factors which may lead to an increase of serum TNF-α level such as infections, liver diseases, diabetes mellitus and autoimmune diseases.
This study included 50 lichen planus patients (36 with cutaneous only lichen planus disease and 14 with oral and cutaneous disease) and 30 healthy controls. All studied individuals were subjected to history taking and clinical examination; we investigated serum level of TNF- with variable parameter including oral and cutaneous lesions, type of cutaneous lesions, age of the patient and duration of the disease.
The result of this work showed the following:
1Elevation of serum level of TNF- in patients with cutaneous lichen planus.
2.Elevation of serum level of TNF- in patients with oral lichen planus.
3.Elevation of serum level of TNF- in patients with oral lichen planus than in patients with cutaneous lichen planus
4.Elevation of serum level of TNF- in patients with lichen planus older than 45 years old than in patients with lichen planus between 16-30 years old.
5.Elevation of serum level of TNF- in female patients with lichen planus than in male patients with lichen planus.
6.Elevation of serum level of TNF- in patients with hypertrophic lichen planus than in patients with common lichen planus, and this elevation is a statistically significant.
7.Serum level of TNF- in patients with actinic lichen planus than is lower than serum level of TNF- in patients with other types of lichen planus.
Conclusion:
Serum level of TNF- was elevated in patients with lichen planus; this supports the fact that TNF- is an important mediator of the pathogenetical process of lichen planus. It is essential for the expression of adhesion molecules; which is important for cell interaction between keratinocytes and T-lymphocytes and this interaction is essential for perpetuation of the disease process.