Update on Connective Tissue Diseases in Dermatology

Abstract

Recent advances in understanding the pathogenesis of autoimmune diseases, including lupus erythematosus, dermatomyositis, and scleroderma, have allowed for reorganization of the classification of these disorders. With these novel stratifications, early identification of rheumatic skin diseases with systemic implications and consistency in designing and executing therapeutic trials will be enhanced. This review will provide a compilation of updates on epidemiology, pathology, evaluation, and classification with a predominant focus on therapeutics, reflecting the growth is this area.

Dental implants in patients with rheumatoid arthritis: clinical outcome and peri‐implant findings

“…Diagnosis of RA was based on the criteria of American Rheumatism Association (ARA), which were fulfilled by 34 patients (Pincus 2005, Costner & Grau 2006). CTDs were diagnosed as a concomitant disease together with RA ( n =9).…”

Cutaneous Connective Tissue Diseases: Epidemiology, Diagnosis, and Treatment

“…Cuticular abnormalities are often observed, such as telengiectasia and erythema in the proximal nail fold. Rare features include bullae on sun-exposed skin, and toxic epidermal necrolysis-like lesions with insidious onset [21, 22]. About 95% of ACLE patients are positive for anti-nuclear antibodies (ANA), including anti-dsDNA, Smith, Ro, or La [18].…”

“…The pathogenesis remains unknown, although supporting evidence is building for a model of immune-mediated destruction of muscle in association with apoptotic reactions leading to skin lesions. Recent evidence has implicated complement components in the development of vascular pathology associated with DM [22]. Elevated C5b-9 deposition in vessels was found in biopsies from DM patients, suggesting the possibility of humoral and complement-mediated damage of endothelium and kertinocytes in DM [22].…”

“…Recent evidence has implicated complement components in the development of vascular pathology associated with DM [22]. Elevated C5b-9 deposition in vessels was found in biopsies from DM patients, suggesting the possibility of humoral and complement-mediated damage of endothelium and kertinocytes in DM [22]. Wenzel and colleagues have observed increased expression of M×A protein, along with cytokine profile suggestive of enhanced Th1 activation in DM patients [31].…”

“…Other systemic manifestations include proximal muscle weakness, dyspnea, dyphagia, arrhythmia, and dyphonia [21]. Diagnosis is validated through laboratory tests revealing increased muscle enzymes such as creatine kinase, aldolase, aspartate aminotransferase, and/or lactate dehydrogenase [22]. Arthralgias are found in nearly 25% of patients exhibiting inflammatory myopathy and usually present with morning joint stiffness [32].…”