Chronic wounds encompass a myriad of lesions, including venous and arterial leg ulcers, diabetic foot ulcers (DFUs), pressure ulcers, non-healing surgical wounds and others. Despite the etiological differences, chronic wounds share several features at a molecular level. The wound bed is a convenient environment for microbial adherence, colonization and infection, with the initiation of a complex host–microbiome interplay. Chronic wound infections with mono- or poly-microbial biofilms are frequent and their management is challenging due to tolerance and resistance to antimicrobial therapy (systemic antibiotic or antifungal therapy or antiseptic topicals) and to the host’s immune defense mechanisms. The ideal dressing should maintain moisture, allow water and gas permeability, absorb wound exudates, protect against bacteria and other infectious agents, be biocompatible, be non-allergenic, be non-toxic and biodegradable, be easy to use and remove and, last but not least, it should be cost-efficient. Although many wound dressings possess intrinsic antimicrobial properties acting as a barrier to pathogen invasion, adding anti-infectious targeted agents to the wound dressing may increase their efficiency. Antimicrobial biomaterials may represent a potential substitute for systemic treatment of chronic wound infections. In this review, we aim to describe the available types of antimicrobial biomaterials for chronic wound care and discuss the host response and the spectrum of pathophysiologic changes resulting from the contact between biomaterials and host tissues.

The human papillomavirus (HPV) belongs to the Papillomaviridae family of viruses which includes small, double-stranded DNA viral agents. Approximately 90% of HPV infections occur asymptomatically and resolve spontaneously. However, infection with high-risk viral strains can lead to the development of preneoplastic lesions, with an increased propensity to become cancerous. The location of these malignancies includes the oral cavity, cervix, vagina, anus, and vulva, among others. The role of HPV in carcinogenesis has already been demonstrated for the aforementioned neoplasia. However, regarding skin malignancies, the mechanisms that pinpoint the role played by HPV in their initiation and progression still elude our sight. Until now, the only fully understood mechanism of viral cutaneous oncogenesis is that of human herpes virus 8 infection in Kaposi sarcoma. In the case of HPV infection, however, most data focus on the role that beta strains exhibit in the oncogenesis of cutaneous squamous cell carcinoma (cSCC), along with ultraviolet radiation (UVR) and other environmental or genetic factors. However, recent epidemiological investigations have highlighted that HPV could also trigger the onset of other non-melanocytic, for example, basal cell carcinoma (BCC), and/or melanocytic skin cancers, for example, melanoma. Herein, we provide an overview of the role played by HPV in benign and malignant skin lesions with a particular focus on the main epidemiological, pathophysiological, and molecular aspects delineating the involvement of HPV in skin cancers.