Biological role of postoperative low level laser therapy in preventing hydroxyapatite orbital implantation exposure: A case report
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- Published online on: February 3, 2021 https://doi.org/10.3892/etm.2021.9745
- Article Number: 314
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Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Conjunctival sac stenosis is the contraction of the conjunctival sac as a result of trauma or disease. The aim of the present study was to observe the clinical effects of low‑level laser therapy (LLLT) combined with hydroxyapatite (HA) orbital implantation as a treatment strategy for conjunctival sac stenosis. A total of 10 patients with conjunctival sac stenosis were treated with scleral graft transplantation in conjunction with HA implantation and postoperative LLLT. In addition, a rabbit model was used to investigate the biological mechanism underlying the effects of LLLT with the aim of preventing and treating orbital implantation exposure. The right eyeball was removed, orbital implantation performed and LLLT applied to experimental groups. 99mTc‑Methyl diphosphonate scanning methods were performed at different timepoints to compare the average radioactivity count of the region of interest between surgical (right) and control (left) eyes (R/L). Histopathological examination was performed 8 weeks post‑surgery, followed by analysis of fiber vascularization. Following LLLT, moderate conjunctival wounds were completely healed within 2 weeks and severe stenosis wounds healed within 3 weeks. Following prosthesis implantation in the rabbit model, a significantly elevated R/L ratio was observed after 4 weeks, whereas no significant difference was observed compared with the control group at 6 and 8 weeks postoperatively. Histopathological examination revealed that all implants were fibrotic. Overall, the present study demonstrated that LLLT promoted the survival of conjunctival grafts, stimulated conjunctival incision healing and promoted early vascularization of HA implants. Clinical trial registration no: ChiCTR‑DDT‑12002660 (www.chictr.org/cn/).
