Enhanced Scar Reduction With Triamcinolone Acetonide and Botulinum Toxin A Combination Therapy Compared to Botulinum Toxin A Monotherapy: A Translational Pilot Study.

[BACKGROUND] The efficacy of combining triamcinolone acetonide (TAC) and botulinum toxin type A (BTX-A) to treat hypertrophic scars and keloids remains unclear.

[OBJECTIVES] This pilot study aimed to compare the clinical efficacy of BTX-A monotherapy and TAC + BTX-A combination therapy in improving scar conditions and to investigate potential mechanisms with a rat burn scar model.

[METHODS] This study was conducted between March 2022 and December 2024. Each patient's scar was randomly divided into 2 equal parts, with 1 part receiving TAC + BTX-A and the other BTX-A alone for 3 sessions at 4-week intervals. Scar thickness was measured with calipers, and the Vancouver Scar Scale (VSS) was administered to assess scar condition. Pain and pruritus were evaluated with a numeric rating scale (NRS) and visual analog scale (VAS), respectively, before each intervention (V1, V2, V3) and 4 weeks after the last session (V4). In the animal study, rats with burn scars were assigned to 5 groups: sham, untreated burn, TAC, BTX-A, and TAC + BTX-A. Scar thickness and expressions of alpha smooth muscle actin (α-SMA), transforming growth factor beta (TGF-β), connective tissue growth factor (CTGF), collagen I/III, laminin, and fibronectin were analyzed histologically.

[RESULTS] Clinically, both therapies reduced scar thickness, VSS, NRS, and VAS scores. However, combination therapy showed superior reductions in scar thickness (V2-V4) and VSS scores (V3, V4) compared to BTX-A monotherapy. No significant differences were observed in NRS and VAS scores. The animal study confirmed that combination therapy more effectively reduced scar thickness, TGF-β and CTGF levels, and the collagen I/III ratio, and increased the laminin/fibronectin ratio.

[CONCLUSIONS] TAC + BTX-A combination therapy enhances scar reduction by more effectively suppressing fibroblast proliferation and activation through TGF-β and CTGF downregulation, promoting scar remodeling.