cheilitis/protease

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Increased mast cell density and protease content in actinic cheilitis.

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BACKGROUND Actinic cheilitis (AC) is a pre-malignant lesion caused by ultraviolet (UV) radiation and characterized by epithelial and connective tissue alterations. Mast cells (MCs), key contributors to solar elastosis in murine UV-irradiated skin, were characterized in order to assess their

Protease inhibitor-related paronychia, ingrown toenails, desquamative cheilitis and cutaneous xerosis.

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Eruptive cheilitis: a new adverse effect in reactive HIV-positive patients subjected to high activity antiretroviral therapy (HAART). Presentation of six clinical cases.

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A variety of exfoliative cheilitis has been observed in reactive HIV-1 patients subjected to high activity antiretroviral therapy (HAART). The lesions exhibit exfoliation, crater formation, fissuring, erosions and/or the formation of papules, vesicles and blisters associated to erythema and edema.

Actinic cheilitis: epithelial expression of COX-2 and its association with mast cell tryptase and PAR-2.

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Cyclooxygenase-2 (COX-2) is overexpressed in various types of human malignancies, including oral cancers. Recent studies have shown that mast cell-derived protease tryptase can induce COX-2 expression by the cleavage of proteinase-activated receptor-2 (PAR-2). Actinic cheilitis (AC) is a

Expression of protease-activated receptor-1 and -2 in orofacial granulomatosis.

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OBJECTIVE Orofacial granulomatosis (OFG) is a rare condition characterized by non-caseating granulomas in the orofacial region. Protease-Activated Receptors (PARs) play a role in inflammatory diseases in diverse human tissues. The aim of the study was to investigate the expression of PAR-1, PAR-2,

Loss-of-function mutations in CAST cause peeling skin, leukonychia, acral punctate keratoses, cheilitis, and knuckle pads.

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Calpastatin is an endogenous specific inhibitor of calpain, a calcium-dependent cysteine protease. Here we show that loss-of-function mutations in calpastatin (CAST) are the genetic causes of an autosomal-recessive condition characterized by generalized peeling skin, leukonychia, acral punctate

Indinavir-induced retinoid-like effects: incidence, clinical features and management.

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Since 1998, many cases of antiretroviral therapy-related paronychia of the toes or fingers and ingrown toenails have been reported. Most of them were related to indinavir. Other indinavir-induced mucocutaneous disorders resembling the adverse effects of systemic retinoid therapy have also been

Cutaneous side effects induced by indinavir.

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HIV-protease inhibitors demonstrated such high efficacy in short-term studies that they have been approved by the FDA, even though possible toxicity still needs further investigation. In the period between January 1997 and August 1998, 101 patients, staying at San Patrignano Medical Centre (Italy),

Fibrinogenolytic and fibrinolytic activity in oral microorganisms.

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Samples were taken from blood accumulated in dental alveoli after surgical removal of mandibular third molars, from subgingival plaque of teeth with advanced periodontal destructions, from teeth with infected necrotic pulps, and from subjects suffering from angular cheilitis. Of the microorganisms

Orofacial effects of antiretroviral therapies.

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This paper summarises some of the oral adverse effects of antiretroviral agents. Some are related to bone marrow suppression which may also predispose to mouth ulcers. Erythema multiforme and toxic epidermal necrolysis are especially well recognized in HIV disease, particularly as reactions to

PLACK syndrome resulting from a novel homozygous variant in CAST

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PLACK syndrome (OMIM 616295) is a form of generalized peeling skin syndrome (GPSS; OMIM 270300). It is an autosomal recessive genodermatosis caused by pathogenic mutations in CAST, which encodes calpastatin, an endogenous specific inhibitor of calpain, a calcium-dependent cysteine protease. We

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