Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy, Including Surgery, Followed by Radiation and Corticosteroid Tape/Plaster

Keloids and hypertrophic scars are fibroproliferative disorders of the skin. Research over the last decade has markedly improved our understanding of the pathogenesis of these scars, in particular, the fact that both disorders are caused by prolonged inflammation that prevents the orderly healing of injured or irritated skin. This protracted inflammatory response is due to genetic, systemic, and local risk factors. Genetic factors include single nucleotide polymorphisms, while systemic factors include hypertension, pregnancy-related and other hormones, and aberrant cytokine levels. An important local factor is the mechanical force (tension) on the scar. These observations have greatly aided the development of therapies for these once-intractable scars. As a result, these scars are now regarded as being completely treatable. At present, we believe that the following combination of three therapies most reliably achieves a complete cure: surgery followed by radiation and the prolonged daily use of corticosteroid tape/plaster

Keloids and Hypertrophic Scars: Update and Future Directions

Summary: The development of cutaneous pathological scars, namely, hypertrophic scars (HSs) and keloids, involves complex pathways, and the exact mechanisms by which they are initiated, evolved, and regulated remain to be fully elucidated. The generally held concepts that keloids and HSs represent “aberrant wound healing” or that they are “characterized by hyalinized collagen bundles” have done little to promote their accurate clinicopathological classification or to stimulate research into the specific causes of these scars and effective preventative therapies. To overcome this barrier, we review here the most recent findings regarding the pathology and pathogenesis of keloids and HSs. The aberrations of HSs and keloids in terms of the inflammation, proliferation, and remodeling phases of the wound healing process are described. In particular, the significant roles that the extracellular matrix and the epidermal and dermal layers of skin play in scar pathogenesis are examined. Finally, the current hypotheses of pathological scar etiology that should be tested by basic and clinical investigators are detailed. Therapies that have been found to be effective are described, including several that evolved directly from the aforementioned etiology hypotheses. A better understanding of pathological scar etiology and manifestations will improve the clinical and histopathological classification and treatment of these important lesions

Primary Ciliary Signaling in the Skin—Contribution to Wound Healing and Scarring

Primary cilia (PC) are solitary, post-mitotic, microtubule-based, and membrane-covered protrusions that are found on almost every mammalian cell. PC are specialized cellular sensory organelles that transmit environmental information to the cell. Signaling through PC is involved in the regulation of a variety of cellular processes, including proliferation, differentiation, and migration. Conversely, defective, or abnormal PC signaling can contribute to the development of various pathological conditions. Our knowledge of the role of PC in organ development and function is largely based on ciliopathies, a family of genetic disorders with mutations affecting the structure and function of PC. In this review, we focus on the role of PC in their major signaling pathways active in skin cells, and their contribution to wound healing and scarring. To provide comprehensive insights into the current understanding of PC functions, we have collected data available in the literature, including evidence across cell types, tissues, and animal species. We conclude that PC are underappreciated subcellular organelles that significantly contribute to both physiological and pathological processes of the skin development and wound healing. Thus, PC assembly and disassembly and PC signaling may serve as attractive targets for antifibrotic and antiscarring therapies.Peer reviewe