IMMUNOHISTOCHEMICAL STUDY OF Ki-67 ANTIGEN EXPRESSION IN DIAGNOSIS OF PSORIASIS

Background: Psoriasis is a common, chronic inflammatory skin disease characterized by scaly white papules and pinpoint bleeding on scratching. Presence of keratinocyte hyperproliferation and abnormal differentiation in the epidermis are some significant features. Histopathologically, it is difficult for the dermatopathologists to differentiate psoriasis from psoriasiform dermatitis when there is a lack of typical features. Aims: To study the Ki-67 antigen expression in the different layers of epidermis of psoriatic skin lesion and its utility in the diagnosis and to differentiate psoriasis from other psoriasiform dermatitis by studying the distribution pattern of Ki-67 immunostaining. Methods: In this cross-sectional study, a total of 91 skin lesions which were clinically labelled as psoriasis and psoriasiform dermatitis were studied, which was confirmed by histopathological examination and followed by Ki-67 immunostaining. The distribution of Ki-67 immunostaining in the supra-basal layer, basal layer and whole epidermis was studied. Results: Ki67 staining was significantly higher in the suprabasal layer and whole epidermis in psoriatic lesions compared to psoriasiform dermatitis. The suprabasal Ki-67 mitotic index was also significantly higher in psoriasis group than psoriasiform dermatitis (p <0.05). We found that in psoriasis > 50% Ki-67 positive keratinocytes are scattered in the suprabasal layer of the epidermis in comparison to the psoriasiform dermatitis which is < 50%. Conclusion: We suggest that Ki-67 labelling index can be used for diagnosing psoriasis and also can differentiate it from other psoriasiform dermatitis.

NOX2 Expression Is Increased in Keratinocytes After Burn Injury

Reepithelialization is crucial for effective wound repair in burn wounds. Reactive oxygen species (ROS) have shown to be important in this. Recent studies suggest that NOX proteins produce ROS in keratinocytes. In the present study, we have studied NOX proteins in burn wounds, including the effect of C1-esterase inhibitor (C1inh) hereon, which is the endogenous inhibitor of complement activity whereof we have shown previously that it also increased the rate of reepithelialization in burn wounds. Skin tissue derived from healthy control Wistar rats (n = 6) were compared with burn-injured rats, with (n = 7) or without C1inh treatment (n = 7). After 14 days, rats were terminated. From the burn-injured rats, the entire wound and nonburned skin from the hind leg, that is, internal control was excised. From the control rats, dorsal skin was excised. In these skin samples, NOX2 and NOX4 were analyzed immunohistochemically. In nonburned rats, NOX2 was found in keratinocytes in both the basal layer and suprabasal layer of the epidermis; and the number of NOX2-positive keratinocytes was 367/mm2 (254–378). In burned rats, the number of NOX2-positive keratinocytes was significantly increased in the newly forming epidermis in the burned area to 1019/mm2 (649–1172), especially in the suprabasal layer, but significantly decreased in remote nonburned skin to 22/mm2 (6–89). C1inh treatment counteracted these changes in epidermal NOX2 expression in burned rats, both in the burned area as in remote nonburned skin. No NOX4 expression was found in the epidermis in none of the groups. NOX2 expression was increased in keratinocytes in newly forming epidermis after burn injury. C1inh, a drug that increases the rate of reepithelialization, counteracted this effect. These results suggest a role for NOX2 in the reepithelialization of burn wounds.

Expression of Cytokeratins 13 and 16 in Middle Ear Cholesteatoma

The accumulation of keratinizing epithelium in the middle ear cavity is a crucial factor in the pathogenesis of cholesteatoma. We hypothesize that keratinocytes from the skin of the ear canal migrate and hyperprollferate in response to Inflammation in the middle ear cavity to cause accumulation of keratin debris. In the present study, we Investigated the expression of specific cytokeratins (CKs) in the cholesteatoma matrix to determine whether cholesteatoma is a hyperproliferative disease. Cytokeratin expression was examined in cholesteatoma, meatal skin, and tympanic membrane with two monoclonal antibodies, one for both cytokeratins 13 and 16 (antibody K8.12), and another for cytokeratin 13 only (antibody K5–1A3). CK 13 (MW 51 KD) Is a marker of differentiation and CK 16 (MW 48 KD) is a marker of hyperproliferatlon of keratinocytes. The use of immunoblot probes showed that CKs 13 and 16 were present in cholesteatoma. Immunofluorescenf staining showed the presence of CK 16 In the suprabasal layer of cholesteatoma, which was located near the external ear canal. CK 16 was also localized in the suprabasal layer of meatal skin and tympanic membrane. CK 13 was localized in the basal layer of the cholesteatoma, distal to the external ear canal, but not in the meatal skin and tympanic membrane. Taken together, the present data suggest that cholesteatoma is a hyperprollferative disease and that cholesteatoma expresses CK 16 near the external ear canal and transforms to express CK 13 during growth distally.