Glucocorticoids are major therapeutic agents highly used in the medical field. Topical glucocorticoids have biologic activities which make them useful in dermatology – anti-inflammatory, vasoconstrictive, immune suppressive and antiproliferative, in treating inflammatory skin disorders (allergic contact eczema, atopic hand eczema, nummular eczema, psoriasis vulgaris or toxic-irritative eczema). Unfortunately, the beneficial effects of topical glucocorticoids are shadowed by their potential for adverse effects – muscle or skin atrophy, striae distensae, rubeosis or acne. Skin atrophy is one of the most prevalent side-effects, with changes found in all skin compartments – marked hypoplasia, elasticity loss with tearing, increased fragility, telangiectasia, bruising, cutaneous transparency, or a dysfunctional skin barrier. The structure and function of the epidermis is altered even in the short-term topical glucocorticoid treatment; it affects stratum corneum components, subsequently affecting skin barrier integrity. The dermis is altered by directly inhibiting fibroblast proliferation, reducing mast cell numbers, and loss of support; there is depletion of mucopolysaccharides, elastin fibers, matrix metalloproteases and inhibition of collagen synthesis. Atrophogenic changes can be found also in hair follicles, sebaceous glands or dermal adipose tissue. Attention should be paid to topical glucocorticoid treatment prescription, to the beneficial/adverse effects ratio of the chosen agent, and studies should be oriented on the development of newer, innovative targeted (gene or receptor) therapies.

Basal cell carcinoma (BCC) is one of the most common malignant tumors worldwide, involving the skin. It is also part of keratinocyte carcinomas, alongside its squamous counterpart. It has low mortality and extremely low metastatic rates (although when present, it indicates a poor patient prognosis); it also has a high morbidity rate through local destruction and recurrence, particularly when perineural invasion is observed, clinically or histopathologically. BCC development is the result of environmental and patient factors, with genetics and ultraviolet radiation playing major roles. The clinical and histopathological aspects vary according to tumor subtype, being classified as high‑risk tumors (nodular, superficial, pigmented and infundibulocystic BCC with adnexal differentiation) and fibroepithelial subtypes, or as high‑risk tumors (micronodular, infiltrating, sclerosing/morphoeic and basosquamous subtype or the type with sarcomatoid differentiation). Dermoscopy is now complimented by novel in vivo diagnostic tools (optical coherence tomography, reflectance confocal microscopy, high‑resolution ultrasonography, Raman spectroscopy or terahertz pulse imaging), improving the diagnostic accuracy and providing tumor depth and lateral margins without the use of invasive techniques. Novel treatment approaches for the treatment of BCC have recently been investigated with the use of hedgehog pathway inhibitors, such as Vismodegib. These approaches aim for complete resolution, minimal side‑effects, high patient satisfaction with the optimal cosmetic results, particularly in key areas, such as the face. The present review article summarizes and discusses the comprehensive clinical and histopathological aspects of BCC, and presents novel imaging tools and therapeutic approaches that have been identified.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder with high prevalence and a complex pathophysiology. This relapsing and remitting skin disorder has many negative consequences on the patient’s quality of life and that of his family. Until now, moderate-to-severe AD treatment was a symptomatic one, using skin emollients, topical corticosteroids, phototherapy, antihistamines and systemic drugs – immune suppressants and other systemic treatments (dupilumab). Starting from 2021, abrocitinib, a Janus kinase-1 inhibitor, was approved for the treatment of moderate-to-severe cases of AD in Europe, in adults. Multiple phase three studies (JADE MONO-1 [NCT03349060]; JADE MONO-2 [NCT03575871]; JADE TEEN [NCT03796676]; JADE COMPARE; GOODERHAM; JADE EXTEND) have yielded positive results in adults and adolescents suffering from this disease, with efficacy, a good tolerance, safe profile, and with generally mild side effects. The positive results were obtained even starting from the first stages of the oral drug administration. The low frequency of side effects and the advantage of having an orally administered medication makes abrocitinib an important additional tool for the treatment of moderate-to-severe forms of AD.

Purpose: The identification of sports and physical exercises with injury risk is necessary to preserve the capacity of athletes and people who perform physical education and also to prevent the installation of functional deficiencies. Methods: We have selected the articles related to the pathogenic mechanisms involved in musculotendinous and fascial injuries produced as a result of physical exercise. Results and Discussions: The lesional pathogenesis is complex and incompletely clarified. Recent theories put in a new light the mechanisms of muscle pain and tendinopathy production. The accumulation of lactate anion, known to be a residue that induces fatigue and muscle pain, has been reconsidered by some authors. It appears that lactate anion is an excellent fuel for the myocardial fiber. Moreover, the accumulation of lactic acid after intense physical exercise could prevent the inexcitability of the sarcolemma induced by the increased concentration of interstitial K⁺. Most of the time, overuse injuries are not limited to muscles. They can cause myofascial, myotendinous or purely muscular injuries. The muscular fascia is more susceptible to injuries produced under the action of large external forces. Also, fascia is more sensitive to pain compared to muscle when external forces act eccentrically. Overloading the tendon and putting it under tension repeatedly is followed by ruptures of the tendon fibers. The regeneration of the degenerated tendon is defective in the context of the inflammation produced by the injury. Tendon fibers undergo a process of fibrosis, scarring, adhesion and heterogeneous calcification. Oxidative stress is responsible for inflammation, degeneration and apoptosis of tenocytes. Conclusion: The benefits brought by physical education and sports are indisputable, but their practice requires a coordinated program to prevent possible traumatic and overuse injuries.

Purpose: Systemic sclerosis (SSc) is a relatively rare collagenosis manifested as microvasculopathy, excessive cutaneous and visceral fibrosis in a background of autoimmune alteration. Autoimmune vasculopathy in SSc occurs early and begins with endothelial cell activation followed by blood vessel intimal proliferation in a context of defective angiogenesis. The alteration of peripheral micro and macrocirculation in SSc is evident through vascular lesions, such as Raynaud’s phenomenon, telangiectasias, acrocyanosis, digital ulcers, gangrene, peripheral pulse deficiency. Our paper details the results of the study on the association between telangiectasias and other types of immune-mediated peripheral vascular lesions that can be identified in SSc. The presence of these peripheral vascular lesions can provide information about the magnitude of the peripheral vasculopathy. Patients and Methods: A total of 37 patients diagnosed with SSc, recruited from a university clinic in Bucharest between February 2019 and March 2020, were enrolled in an observational study. We evaluated the presence of telangiectasias, as a stigma of autoimmune microvasculopathy, and their association with other immune-mediated peripheral vascular lesions that may be present in SSc. Results: The presence of telangiectasias was identified in the absence, but especially in the presence of acrocyanosis and digital ulcerations, and patients with peripheral pulse deficiency almost always had telangiectasias. Less than a quarter of the patients with digital ulcers progressed unfavorably to gangrene, and only one required amputation, telangiectasias being present not only in the patient with amputation but in all patients with gangrene. Conclusion: We appreciate that telangiectasias may be the clinical expression of peripheral vasculopathy characteristic of SSc, they can often be present in association with other peripheral vascular lesions and may represent a valuable indicator for the gangrene risk of digital ulcerations in SSc.