Histopathologic Study of Rosacea and the Role of Demodex Folliculorum
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Abstract:
Background and Objective: Rosacea is a common and ill-defined disease and Demodex folliculorum has been reported in rosacea in a number of clinical studies. Since demodex mite is present in many healthy individuals, the mite may have a pathogenic role only when it is present in high densities. Therefore, in this study, the possible role of demodex folliculorum and the importance of mite density were investigated using an elliptical incisional skin biopsy technique. Materials and Methods: Thirty-nine patients with rocacea, twenty-five females, 14 males, and 41 age- and sex-matched healthy individuals as control were included in the study. With the incisional skin biopsy of face, we studied six sections of each sample. We also studied the number of follicles, mite density, epidermal changes, solar elastosis, inflammatory cells in the dermis and their pattern, granuloma formation, and vascular changes. Results: Varying degree of vasodilatation, solar elastosis, and inflammatory infiltrate were found in all patients. The infiltrate was lympho-histiocytic in 29 cases, lympho-plasmacytic in 6 cases, neutrophilic, especially around hair follicles in 2 cases, and eosinophilic infiltration mixed with mononuclear cells in 2 cases. The number of D. folliculorum was statistically significant. There was also a significant difference between males and females regarding the number of mite in rosacea in relation to age (p = 0.047). There was also granuloma around appendages in 3 cases and granuloma around hair follicle in 2 cases. One case in the latter group had degenerated demodex cuticle. Conclusion: Rosacea is a multifactorial disease and high densities of demodex are important in the form of hypersensitivity reaction to antigens or granuloma formation in response to its cuticle or destructed hair follicles. The individual properties may modify the severity of inflammatory response to demodex.
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Journal title
volume 1 issue 4
pages 169- 172
publication date 2006-09-01
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