The triggers for cholesteatoma onset are diverse, and may involve tympanic membrane trauma (i.e. perforation, displacement, retraction or invagination), tympanic membrane disease, and/or tympanic cavity mucosa disease. Research has revealed that cell migration is replaced under inflammatory conditions by hyperplasia, which triggers the onset of cholesteatoma. Lately, the hyperplasia theory gained prominence and circumscription of the papillary cone formation concept provided insight into cholesteatoma progression (growth and expansion). Diseased mucosa can contribute to the development of retraction pockets and cholesteatoma. The type of cholesteatoma trigger and the role of chronic inflammation during disease progression and recurrence are important in guiding clinical intervention.

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For centuries, keloids have been an enigma and despite considerable research to unravel this phenomenon no universally accepted treatment protocol currently exists. Historically, the etiology of keloids has been hypothesized by multiple different theories; however, a more contemporary view postulates a multifactoral basis for this disorder involving nutritional, biochemical, immunological, and genetic factors that play a role in this abnormal wound healing. Critical to the process of preventing or managing keloids is the need to locally control fibroblasts and their activities at the wound site. In recent years, considerable evidence has accumulated demonstrating the importance of fatty acids and bioactive lipids in health and disease, especially those involving inflammatory disorders or immune dysfunction. If hypertrophic scarring and keloid formation can be argued to have significant inflammatory histories, then it is possible to postulate a role for lipids in their etiology and potentially in their treatment. This report briefly visits past views and theories on keloid formation and treatment, and offers a theoretical rationale for considering adjuvant fatty acid therapy for keloid management. Sufficient scientific evidence in support of fatty acid strategies for the prevention and treatment of keloids currently exists, which offer opportunities to bridge the gap between the laboratory and the clinic. The intent of this paper is to serve as a basic guideline for researchers, nutritionists, and clinicians interested in keloids and to propose new directions for keloid management.

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