Keloids are benign fibroproliferative tumors more frequently found among African Americans. Until now, keloid etiopathogenesis is not fully understood. To characterize keloids in African Americans, we performed transcriptional profiling of biopsies from large chronic keloids, adjacent nonlesional (NL) skin (n=3) and a newly formed keloid lesion using Affymetrix HGU133 2.0 plus arrays. Quantitative RT-PCR (qRT-PCR) and immunohistochemistry staining were done to confirm increased expression of relevant genes. We identified 1,202 up-regulated and 961 down-regulated differentially expressed genes (DEGs) between keloid and NL skin; 1,819 up- and 1,867 down-regulated DEGs between newly formed keloid and NL skin; and 492 up- and 775 down-regulated DEGs between chronic and newly formed keloid (Fold change >2, False discovery rate <0.05). Many of the top up-regulated DEGs between chronic keloid and NL skin, and between newly formed keloid and NL skin are involved in bone/cartilage formation including Fibrillin 2(FBN2), Collagen type X alpha1(COL10A1), Asporin(ASPN), Cadherin 11(CDH11), Bone morphogenic protein 1(BMP1), Secreted phosphoprotein 1(SPP1), and Runt-related transcription factor2(RUNX2). qRT-PCR confirmed significant (p<0.05) up-regulation of BMP1, RUNX2, CDH11 and FBN2 in chronic keloid compared to NL skin. Immunohistochemistry staining showed increased protein expression of ASPN, CDH11, BMP1 and RUNX2 on chronic and newly formed keloid compared to NL skin. Our study shows that large keloids in African Americans represent a dysplasia of cutaneous connective tissue towards immature cartilage or bone differentiation. The phenotype is potentially regulated by overexpression of RUNX2. This knowledge may give insights to guide the development of better treatment for the disease in the future.

Keloid disorder (KD) is a fibroproliferative ailment of the cutaneous connective tissue secondary to dysregulation in various skin repair and healing processes. This disorder is characterized by excess collagen and/or glycoprotein depositions in the dermis. Age of onset of KD is not well documented. Based on clinical observations, various authors have reported the onset of KD to be between the ages of 10 and 30 years. We report on an African American female who developed bilateral auricular keloids at the age of 9 months. To our knowledge, this is the youngest age at which a patient has been documented to have developed KD.

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Keloid disorder is one of the most frustrating problems in wound healing and advances in our understanding of the differences of occurrence at a single site versus multiple sites might help in understanding pathogenesis and improving treatment.

Importance: Health care providers have long struggled with recurrent and hard to treat keloids. Advancing our understanding of natural history and risk factors for development of large, very large and massive neck keloids can lead to improved treatment outcomes. Clinical staging system for the categorization of keloid lesions, as well as grouping of keloid patients according to the extent of skin involvement is both fundamental for design and delivery of proper plan of care and an absolute necessity for methodical trial design and interpretation of the results thereof. Objective: To review clinical presentation and natural history of neck keloids; to explore risk factors for development of large, very large and massive neck keloids; and to propose a clinical staging system that allows for categorization of keloid lesions by their size and grouping of keloid patients by the extent of their skin involvement.  Setting: This is a retrospective analysis of 82 consecutive patients with neck keloids who were seen by the author in his keloid specialty medical practice.    Intervention: Non-surgical treatment was offered to all patients.  Results: Neck-area keloids were found to have several unique characteristics. All 65 African Americans in this study had keloidal lesions elsewhere on their skin. Very large and massive neck keloids appear to be race-specific and almost exclusively seen among African Americans. Submandibular and submental skin was the most commonly involved area of the neck. Keloid removal surgery was found to be the main risk factor for development of very large and massive neck keloids.  Conclusions and relevance: Surgical removal of neck keloids results in wounding of the skin and triggering a pathological wound-healing response that often leads to formation of a much larger keloid.  Given the potential for greater harm from surgery, the author proposes non-surgical approach for treatment of all primary neck keloids. Author’s attempts to properly categorize keloid lesions and to group the study subjects was hampered by the lack of a previously defined methodology. A clinical staging system is proposed to address the deficiency in grouping of keloid patients according to the size and extent of skin involvement with keloid lesions.