Use of Intralesional Cryosurgery as an Innovative Therapy for Keloid Scars and a Review of Current Treatments

Keloids are benign growths characterized by excessive collagen formation. The treatment of keloid scars remains a challenging clinical dilemma for both patients and providers. Intralesional cryosurgery has emerged as a safe and effective new treatment by destroying the hypertrophic scar tissue with minimal damage to the skin surface.Keloids are benign, dermal, fibroproliferative tumors characterized by excess collagen at the site of previous skin injury. Keloid scars extend beyond the borders of the original wound in contrast to hypertrophic scars, which are limited to the original wound site. Keloids often develop soon after injury, but can also occur up to several years following the initial traumatic insult.1Keloid scars are well-demarcated, rubbery, mildly tender, bosselated tumors with a shiny surface, often marked by telangectasias and sometimes ulcerations. Lesions are pink to purple in color and may display hyperpigmentation. The most common anatomic sites include the anterior chest, shoulders, ear lobes, cheeks, and skin overlying joints. After development, keloid lesions continue to persist without spontaneous regression and have no malignant potential. Patients often complain of pruritis, pain, and hyperesthesia. These symptoms, along with the contractures from excessive scar formation, can be extremely uncomfortable for patients.2,3A histological examination of a keloid reveals larger, thicker, and more disorganized collagen fibers than those seen in normal skin.1 They are pale-staining, hypocellular type I and III collagen bundles that lack nodules. Blood vessels are scattered and dilated, contributing to the poor vascularization in keloid scars. Special stains can detect the overproduction of fibronectin, an extracellular matrix protein.2Excessive scar formation is due to abnormal wound healing following any injury to the deep dermis. Common causes include surgical procedures, piercings, vaccinations, lacerations, and burn injuries. Normal wound healing depends on the fine balance between extracellular matrix deposition and degradation.2 Over expression of fibroblast-specific growth factors has been implicated in the pathogenesis of keloids; these molecules include vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF). Additionally, keloid scars endure a longer inflammatory period compared to other scars, during which immune cells and pro-inflammatory cytokines continue to stimulate fibroblasts.2,3 Due to these aberrations and imbalances between the anabolic and catabolic phases of wound healing, there is exaggerated fibroblast activity and ultimately increased collagen synthesis.1,3The likelihood of developing a keloid scar is multifactorial with a strong genetic component. There is potential for all individuals (except albinos) to develop keloid scars; however, the greatest incidence is observed in patients of darker skin color. Keloids are most common in the second to third decades of life, and susceptibility decreases with age.2,3