The skin is an organ with multiple functions, where important inflammatory and immunological processes take place. The integrity of the skin barrier is necessary for it to fulfill its roles. An intact skin barrier requires a physiological keratinization process, but also a normal cutaneous microbial flora. Any change in the proliferation and differentiation of keratinocytes entails the disruption of the skin barrier and the triggering of inflammatory and immunological processes at this level, in response to the aggression of external pathogens. Also, there are several specialised immune cells in the skin (Langerhans cells, T regulator cells, T helper cells), that maintain a balance between pro-inflammatory and anti-inflammatory processes at this level. Disturbing the immune homeostasis causes inflammation and allergic skin reaction. Psoriasis and atopic dermatitis are two inflammatory diseases of the skin, characterized by perturbation of the mechanisms of skin barrier formation. The immune system of the skin is also involved in the pathophysiology of vitiligo and pemphigus. The aim of this review is to offer a brief presentation of the inflammatory and immunological processes that occur in the skin.

SummaryAim: The purpose was to identify if rheumatoid arthritis (RA) influenced levels of salivary biomarkers of periodontal disease.Methods: Biological assessments and periodontal examinations were performed in 15 patients with RA, 10 patients with chronic periodontitis and 11 healthy patients as controls. Unstimulated whole salivasamples were analysed for interleukin-1b (IL-1b) and tumour necrosis factor-α (TNF-α) concentrations.Results: The arthritis and healthy patients had significantly less oral disease than the periodontitis group but the arthritis group had significantly moresites bleeding on probing (BOP) than the control group. Salivary levels ofIL-1b were significantly elevated in the periodontal disease group, and IL-1b was the only biomarker with significantly higher levels in the arthritis group compared with control group. Arthritis patients receiving anti-TNF-α antibody therapy had significantly lower IL-1b and TNF-α levels compared with arthritis patients not on the anti-TNF-α therapy and healthy controls, respectively.Conclusion: RA patients have higher levels of periodontal inflammation than healthy control group and also an increased BOP. Systemic inflammation appears to influence levels of selected salivary biomarkers of periodontal disease, and anti-TNF-α therapy significantly modified lowered salivary levels IL-1b and TNF-α levels in RA.

The adrenal gland serve important roles in the modulation of the immune response, the adjustment of blood pressure, the stress reaction via glucocorticoids and the hydroelectrolytic balance via mineralocorticoids. Primary adrenal insufficiency, known as Addison disease, is characterized by a decrease in glucocorticoid secretion (cortisol) and, more rarely, by a hyposecretion of mineralocorticoids (aldosterone). The production of cortisol, which is a hormone that helps the body respond to stress, is regulated in the brain, the hypothalamus and the pituitary gland. The hypothalamus stimulates the pituitary gland to produce adrenocorticotropic hormone, which stimulates cortisol production from the adrenal gland. If left untreated, Addison disease has a high mortality rate. Corticotherapy used in the treatment of Addison disease is associated with a certain cardiovascular risk. The proatherogenic effect of corticoids is based on the chronic inflammatory response of the vascular wall to a series of events. The aim of the current case report was to review the pathophysiological mechanisms and interactions that may lead to the onset of acute coronary syndrome with ST elevation in a patient with Addison disease.

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