Oral diseases are the complex host responses composed of a broad array of inflammatory cells, and cytokines, chemokines, and mediators derived from the cells resident in the gingival tissues, as well as from the emigrating inflammatory cells. A chronic polymicrobial challenge to the local host tissues triggers this response, which under certain circumstances, and in a subset of the population, leads to the progressing soft and hard tissue destruction that characterizes periodontitis. The red complex has been proposed as a pathogenic consortium, consisting of P. gingivalis, T. denticola, and T. forsythia. This review has attempted to examine the virulence potential and determinants of these commensal opportunists.

Calciphylaxis also known as Calcific uremic arteriolopathy (CUA), is a rare fatal complication usually associated with end-stage renal disease (ESRD). It is characterized by skin ulceration and necrosis leading to significant pain. The disease calciphylaxis is pathological state resulting in accumulation of calcium content in medial wall of small blood vessels along with the fibrotic changes in intima. The aetiopathogenesis of this disease, small vessel vasculopathy, remains complicated, and unclear. It is believed that development of calciphylaxis depends on medial calcification, intimal fibrosis of arterioles and thrombotic occlusion. The disease is rare, life-threatening medical condition that occurs mostly in population with kidney disease or in patients on dialysis. Skin biopsy and radiographic features are helpful in the diagnosis of calciphylaxis, but negative results do not necessarily exclude the diagnosis. This article highlights steps undertaking in the diagnosis of calciphylaxis.

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