OBJECTIVES/HYPOTHESIS: Unilateral vocal fold paralysis (UVFP) induces hoarseness due to progressive atrophy of the denervated thyroarytenoid (TA) muscle. Therefore, treatments aimed at regenerating the atrophied TA muscle are required. Basic fibroblast growth factor (bFGF) is involved in muscle development and regeneration. This study aimed to elucidate the effects of bFGF injection on atrophied TA muscle. STUDY DESIGN: Animal research. METHODS: A recurrent laryngeal nerve-paralysis rat model was established, and low- (200 ng) or high-dose (2,000 ng) bFGF or saline (control) was injected into the TA muscle 28 days later. The larynges were excised on day 1, 3, 7, 14, and 28 after treatment. The cross-sectional area of the TA muscle in normal and paralyzed sides was compared, and the Ki67-positive (Ki67+ ) dividing cells, paired box 7-positive (Pax7+ ) satellite cells (SCs), and myogenic differentiation-positive (MyoD+ ) myoblasts were counted. RESULTS: The TA muscle area of animals administered high-dose bFGF increased with time and was significantly larger than that of the saline-injected controls 28 days after treatment (P < .05). The counts of Ki67+ and Pax7+ cells were the highest on day 1, whereas the MyoD+ myoblast count was highest on day 7. These results suggest that bFGF administration into the denervated TA muscles compensated for the atrophied TA muscles by inducing proliferation of SCs and their differentiation to myoblasts. CONCLUSIONS: A single injection of high-dose bFGF augmented regeneration and differentiation of the atrophied TA muscle by enhancing proliferation and differentiation of muscle SCs, suggesting its possible clinical application in humans with UVFP. LEVEL OF EVIDENCE: NA Laryngoscope, 130:159-165, 2020.
OBJECTIVES/HYPOTHESIS: Unilateral vocal fold paralysis (UVFP) induces hoarseness due to progressive atrophy of the denervated thyroarytenoid (TA) muscle. Therefore, treatments aimed at regenerating the atrophied TA muscle are required. Basic fibroblast growth factor (bFGF) is involved in muscle development and regeneration. This study aimed to elucidate the effects of bFGF injection on atrophied TA muscle. STUDY DESIGN: Animal research. METHODS: A recurrent laryngeal nerve-paralysisrat model was established, and low- (200 ng) or high-dose (2,000 ng) bFGF or saline (control) was injected into the TA muscle 28 days later. The larynges were excised on day 1, 3, 7, 14, and 28 after treatment. The cross-sectional area of the TA muscle in normal and paralyzed sides was compared, and the Ki67-positive (Ki67+ ) dividing cells, paired box 7-positive (Pax7+ ) satellite cells (SCs), and myogenic differentiation-positive (MyoD+ ) myoblasts were counted. RESULTS: The TA muscle area of animals administered high-dose bFGF increased with time and was significantly larger than that of the saline-injected controls 28 days after treatment (P < .05). The counts of Ki67+ and Pax7+ cells were the highest on day 1, whereas the MyoD+ myoblast count was highest on day 7. These results suggest that bFGF administration into the denervated TA muscles compensated for the atrophied TA muscles by inducing proliferation of SCs and their differentiation to myoblasts. CONCLUSIONS: A single injection of high-dose bFGF augmented regeneration and differentiation of the atrophied TA muscle by enhancing proliferation and differentiation of muscle SCs, suggesting its possible clinical application in humans with UVFP. LEVEL OF EVIDENCE: NA Laryngoscope, 130:159-165, 2020.