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The anal fistula tract is a pathological, epithelialized communication between the anal canal and the perianal skin, typically originating from an infected anal gland or as a complication of Crohn's disease [1]. The sphincter muscle tissue, consisting of the internal and external anal sphincters, surrounds the anal canal and is essential for maintaining fecal continence [4]. In clinical pharmacology and regenerative medicine, the fistula tract and surrounding sphincter tissue are treated as the anatomical site for local therapeutic interventions, such as the injection of expanded adipose-derived mesenchymal stem cells (e.g., darvadstrocel) or the application of fibrin sealants [2][3]. These therapies aim to modulate the local inflammatory environment and promote the closure of the tract while preserving the integrity of the sphincter muscles [3]. While not a single molecular target, the tissue complex is the focus of multi-modal treatments involving both surgical repair and biological agents that target underlying inflammatory pathways [1][2]. The management of this tissue is particularly challenging because aggressive surgical removal of the tract can lead to permanent damage to the sphincter muscles, resulting in fecal incontinence [1]. Consequently, modern drug development focuses on sphincter-sparing techniques that use biological or cellular products to induce healing from within the tract [2].
Local delivery of cellular therapies or surgical sealants to the fistula tract to induce immunomodulation and promote tissue regeneration and closure.
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