Inflammation is often associated with the development and progression of cancer. The cells responsible for cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance; therefore, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammations can result in immunosuppression, thereby providing a preferred background for tumor development. The current review provides a link between inflammation and cancer development.

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.

Dentin dysplasia (DD) is an uncommon developmental disturbance affecting dentin, resulting in enamel with atypical dentin formation and abnormal pulpal morphology. Type I (radicular) and Type II (coronal) are the two types of DD. Type I is more common, and both types include single or multiple teeth in primary and permanent dentition. Combinations of both types have also been described in literature. Four distinct forms of Type I and one form of Type II were identified. This case report documents one such rarity of DD in an 11-year-old female with clinical and radiographical findings and management aspects.

Background and aim: Oxidative stress as an individual risk for periodontitis and chronic kidney disease (CKD) has been elaborated through various mechanical pathways, yet its role in association with both diseases remains unexplored. Thus, the current study aims in evaluating serum glutathione peroxidase, an oxidative stress marker in CKD patients with periodontitis, and compare it with the healthy controls.Methodology: One hundred and twenty subjects were divided into four groups as control (C=30 subjects), periodontitis and non-CKD patients (CP=30 patients), non-periodontitis and CKD patients (CKD=30 patients), and periodontitis and CKD patients (CKD+CP=30 patients). Demographic variables, periodontal parameters, such as plaque index (PI), gingival index (GI), probing pocket depth (PPD), percentage proportion of sites with probing pocket depth more than 5 mm, clinical attachment loss (CAL), percentage proportion of sites with clinical attachment loss more than 3 mm and serum stress marker, and glutathione peroxidase were compared between the groups and the results were statistically analyzed.Results: The demographic variables did not differ significantly between the groups, except for age. The means PI, GI, PPD, percentage proportion of sites with probing pocket depth more than 5 mm, CAL, percentage proportion of sites with clinical attachment loss were higher in CKD+CP. The glutathione peroxidase was significantly higher in CP group (p=0.001) and significantly correlated with periodontal parameters. Conclusion:The oxidative stress marker glutathione peroxidase was higher in CP, followed by the CKD groups. This could pave a strong link of oxidative stress as a risk factor for chronic periodontitis, as well as chronic kidney disease.

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