Khan Mohd Afzal, Fatima Gehan, Ashiquzzaman Akm, Kim Sang Seong, Kwon Hyuksang, Kim Young Ro, Chung Euiheon
Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Department of Radiology, Harvard Medical School, Boston, Massachusetts.
Ophthalmol Sci. 2024 Dec 18;5(3):100680. doi: 10.1016/j.xops.2024.100680. eCollection 2025 May-Jun.
Neuropathic corneal pain (NCP) is a debilitating condition characterized by persistent pain due to corneal nerve damage or dysfunction. Millions of individuals and their families endure the significant impact of chronic pain. Effective management strategies are crucial yet limited, prompting the exploration of innovative treatments such as photobiomodulation (PBM).
In vivo preclinical therapeutics investigation in mice.
Thy1-YFP mice.
This study evaluates the efficacy of PBM in treating NCP across 4 animal models: normal control, sham control, pulled nerve, and full transection (FT). Behavioral assessments, including the von Frey test (VFT) for mechanical sensitivity and the eye-wiping test (EWT) for chemical sensitivity, were employed to evaluate the therapeutic impact of PBM till day 56 (D-1, D1, D3, D5, D7, D14, D28, D42, and D56).
Advances in therapeutic approach for NCP through the potential of PBM.
Photobiomodulation significantly reduced behavioral manifestations of pain in the pulled nerve model (VFT: no PBM [D1 = 0.043 ± 0.044, D56 = 0.05 ± 0.014] and PBM [D1 = 0.050 ± 0.008 { value = 0.18}, D56 = 0.09 ± 0.014 { value = 0.02}], EWT: no PBM [D1 = 11.96 ± 0.47, D56 = 12.11 ± 0.15] and PBM [D1 = 11.73 ± 0.18 { value = 0.2}, D56 = 11.22 ± 0.31] [ value = 0.01]) and FT model (VFT: no PBM [D1 = 0.022 ± 0.0028, D56 = 0.023 ± 0.0047] and PBM [D1 = 0.024 ± 0.0028 { value = 0.2}, D56 = 0.073 ± 0.0094] [ value = 0.02]), EWT: no PBM [D1 = 13.1 ± 0.14, D56 = 13.36 ± 0.30] and PBM [D1 = 12.86 ± 0.41, { value = 0.2}, D56 = 12.53 ± 0.41] [ value = 0.04]}, suggesting an effective reduction of pain sensitivity and an increase in corneal nerve function. The temporal patterns also suggest that early intervention with PBM, initiated shortly after nerve injury, may be crucial for preventing the chronic progression of NCP.
These outcomes support PBM as a promising nonpharmacologic intervention for NCP; this not only reinforces the potential of PBM in NCP treatment but also provides a foundation for future clinical applications in managing corneal neuropathy.
The author(s) have no proprietary or commercial interest in any materials discussed in this article.
神经性角膜疼痛（NCP）是一种使人衰弱的疾病，其特征是由于角膜神经损伤或功能障碍导致持续性疼痛。数以百万计的患者及其家庭承受着慢性疼痛带来的重大影响。有效的管理策略至关重要，但却有限，这促使人们探索诸如光生物调节（PBM）等创新疗法。
对小鼠进行体内临床前治疗研究。
Thy1-YFP小鼠。
本研究在4种动物模型中评估PBM治疗NCP的疗效：正常对照、假手术对照、牵拉神经和完全横断（FT）。采用行为学评估，包括用于机械敏感性的von Frey测试（VFT）和用于化学敏感性的擦眼测试（EWT），以评估PBM直至第56天（D-1、D1、D3、D5、D7、D14、D28、D42和D56）的治疗效果。
通过PBM的潜力推进NCP的治疗方法。
光生物调节显著降低了牵拉神经模型（VFT：无PBM [D1 = 0.043±0.044，D56 = 0.05±0.014]和PBM [D1 = 0.050±0.008 {值 = 0.18}，D56 = 0.09±0.014 {值 = 0.02}]，EWT：无PBM [D1 = 11.96±0.47，D56 = 12.11±0.15]和PBM [D1 = 11.73±0.18 {值 = 0.2}，D56 = 11.22±0.31] [值 = 0.01]）和FT模型（VFT：无PBM [D1 = 0.022±0.0028，D56 = 0.023±0.0047]和PBM [D1 = 0.024±0.0028 {值 = 0.2}，D56 = 0.073±0.0094] [值 = 0.02]）中疼痛的行为表现，EWT：无PBM [D1 = 13.1±0.14，D56 = 13.36±0.30]和PBM [D1 = 12.86±0.41，{值 = 0.2}，D56 = 12.53±0.41] [值 = 0.04]}，表明疼痛敏感性有效降低，角膜神经功能增强。时间模式还表明，在神经损伤后不久开始的PBM早期干预可能对预防NCP的慢性进展至关重要。
这些结果支持PBM作为一种有前景的NCP非药物干预措施；这不仅强化了PBM在NCP治疗中的潜力，也为未来管理角膜神经病变的临床应用提供了基础。
作者对本文讨论的任何材料均无所有权或商业利益。
