Background: Chronic cutaneous wounds such as diabetic foot ulcers, venous leg ulcers, pressure injuries, and burns remain a global clinical burden. These wounds are often arrested in inflammatory or ischemic stages due to impaired angiogenesis and growth factor deficiencies. Biologic therapies, such as platelet-rich plasma (PRP) and recombinant growth factors, aim to restore these deficits and accelerate repair. Methods: A narrative review of PubMed and Google Scholar (2015–2025) identified 64 English-language studies, including randomized controlled trials, meta-analyses, and translational investigations evaluating PRP and recombinant growth factors in wound healing. Results: Randomized trials and meta-analyses show that adjunctive autologous PRP increases complete wound closure versus standard care in chronic ulcers, including diabetic foot and venous leg ulcers (odds ratios ≈ 2–8), and improves healing rates in pressure injuries (odds ratio ≈ 3.4), without increasing adverse events. In diabetic foot ulcers, PDGF-BB and EGF, together with PRP, consistently improve complete healing and reduce ulcer area. In burns, topical EGF and bFGF shorten healing time by ~3 days in superficial partial-thickness wounds and by >5 days in deeper burns, with generally improved scar outcomes. Conclusions: PRP offers broad, autologous biologic activation, while recombinant growth factors deliver high-potency, targeted precision. Together, they represent complementary regenerative strategies that can shorten healing times and improve outcomes in chronic wounds. Standardized multicenter trials quantifying cytokine composition, cost-effectiveness, and long-term limb-salvage benefit are warranted to guide their integration into routine clinical practice.

Granuloma annulare (GA) is a chronic granulomatous dermatosis that often proves resistant to conventional therapies. Increasing evidence implicates interferon-gamma-mediated JAK-STAT activation in GA pathogenesis, with tyrosine kinase 2 (TYK2) playing a central role through IL-12, IL-23, and type I interferon signaling. Deucravacitinib, a selective allosteric TYK2 inhibitor, has emerged as a potential therapy by targeting these pathways. We present the case of a 59-year-old woman with biopsy-confirmed interstitial-type GA that was unresponsive to topical corticosteroids. Initiation of deucravacitinib 6 mg daily led to complete clearance of lesions within one month. Reported adverse effects were limited to brief episodes of aphthous ulcers during the first two weeks of therapy, which resolved spontaneously. Laboratory testing two weeks after treatment initiation showed mild elevations in lipids and glucose and slightly decreased calcium, though baseline labs were not available for comparison and no serious adverse events occurred. This case highlights the potential of deucravacitinib as a novel therapeutic option for refractory GA and adds to emerging evidence that TYK2 inhibition may represent a targeted and effective approach for this condition.