Objectives: Traumatic optic neuropathy (TON), a relatively rare condition, can cause visual functional impairment and permanent functional damage.Surgeons should be familiar with its diagnostic criteria and treatment to effectively manage cases of facial trauma with TON. We investigated the feasibility of navigation-assisted endoscopic trans-nasal optic nerve decompression (ETOND) to treat TON in maxillofacial trauma patients. Patients and Methods: We retrospectively analyzed data from the clinical investigation of four consecutive patients, two males and two females with an average age of 75 years, with midfacial fractures and TON between April 2021 and September 2023. All patients had swelling and subcutaneous periorbital hemorrhage accompanied by optic nerve canal and zygomaticomaxillary complex fractures on the affected side. Three patients had lacerations on the lateral eyebrow or upper eyelid. All patients were evaluated by an ophthalmologist for visual impairment; two patients could see hand motion at a 30 cm distance, one patient could perceive light, and one did not have any loss of visual acuity. Among the four patients, three had visual impairment immediately after the injury, and one showed delayed impairment. Results: The patients were treated with navigation-assisted ETOND conducted by an endoscopic rhinologist. Three of the ETONDs were performed along with open reduction and internal fixation (ORIF); the other ETOND was delayed. Orbital reconstruction was performed in three patients. Steroid therapy was administered to two patients, one pre-operatively and one post-operatively. The two patients with pre-operative vision loss showed improved visual acuity post-operatively, and the two patients with no pre-operative visual impairment had no vision loss associated with ORIF for their midfacial fractures. No patient had post-operative complications. Conclusion Navigation-assisted ETOND can be performed easily by endoscopic rhinologists; and prompt examination, diagnosis, and treatment are important in patients with facial trauma and TON.

Objectives: Traumatic optic neuropathy (TON), a relatively rare condition, can cause visual functional impairment and permanent functional damage.Surgeons should be familiar with its diagnostic criteria and treatment to effectively manage cases of facial trauma with TON. We investigated the feasibility of navigation-assisted endoscopic trans-nasal optic nerve decompression (ETOND) to treat TON in maxillofacial trauma patients. Patients and Methods: We retrospectively analyzed data from the clinical investigation of four consecutive patients, two males and two females with an average age of 75 years, with midfacial fractures and TON between April 2021 and September 2023. All patients had swelling and subcutaneous periorbital hemorrhage accompanied by optic nerve canal and zygomaticomaxillary complex fractures on the affected side. Three patients had lacerations on the lateral eyebrow or upper eyelid. All patients were evaluated by an ophthalmologist for visual impairment; two patients could see hand motion at a 30 cm distance, one patient could perceive light, and one did not have any loss of visual acuity. Among the four patients, three had visual impairment immediately after the injury, and one showed delayed impairment. Results: The patients were treated with navigation-assisted ETOND conducted by an endoscopic rhinologist. Three of the ETONDs were performed along with open reduction and internal fixation (ORIF); the other ETOND was delayed. Orbital reconstruction was performed in three patients. Steroid therapy was administered to two patients, one pre-operatively and one post-operatively. The two patients with pre-operative vision loss showed improved visual acuity post-operatively, and the two patients with no pre-operative visual impairment had no vision loss associated with ORIF for their midfacial fractures. No patient had post-operative complications. Conclusion Navigation-assisted ETOND can be performed easily by endoscopic rhinologists; and prompt examination, diagnosis, and treatment are important in patients with facial trauma and TON.

Objectives: Traumatic optic neuropathy (TON), a relatively rare condition, can cause visual functional impairment and permanent functional damage.Surgeons should be familiar with its diagnostic criteria and treatment to effectively manage cases of facial trauma with TON. We investigated the feasibility of navigation-assisted endoscopic trans-nasal optic nerve decompression (ETOND) to treat TON in maxillofacial trauma patients. Patients and Methods: We retrospectively analyzed data from the clinical investigation of four consecutive patients, two males and two females with an average age of 75 years, with midfacial fractures and TON between April 2021 and September 2023. All patients had swelling and subcutaneous periorbital hemorrhage accompanied by optic nerve canal and zygomaticomaxillary complex fractures on the affected side. Three patients had lacerations on the lateral eyebrow or upper eyelid. All patients were evaluated by an ophthalmologist for visual impairment; two patients could see hand motion at a 30 cm distance, one patient could perceive light, and one did not have any loss of visual acuity. Among the four patients, three had visual impairment immediately after the injury, and one showed delayed impairment. Results: The patients were treated with navigation-assisted ETOND conducted by an endoscopic rhinologist. Three of the ETONDs were performed along with open reduction and internal fixation (ORIF); the other ETOND was delayed. Orbital reconstruction was performed in three patients. Steroid therapy was administered to two patients, one pre-operatively and one post-operatively. The two patients with pre-operative vision loss showed improved visual acuity post-operatively, and the two patients with no pre-operative visual impairment had no vision loss associated with ORIF for their midfacial fractures. No patient had post-operative complications. Conclusion Navigation-assisted ETOND can be performed easily by endoscopic rhinologists; and prompt examination, diagnosis, and treatment are important in patients with facial trauma and TON.

The mandibular condyle formation during temporomandibular joint (TMJ) development exhibits endochondral bone formation, and the elongation process is dependent on the normal cartilage proliferation and differentiation. Retinoids are important for maturation of growth-plate chondrocytes, but the identity of their downstream effectors remains unclear. In this study, we carried out a series of studies at the cellular, biochemical, and molecular levels to determine whether, and if so how, retinoid signaling is related to the expression and function of Indian hedgehog (Ihh) in chondrocyte proliferation. First we analyzed the RA receptor (RAR) and Ihh expression pattern in E18 mandibular condyle. RARα and RARβ mRNA were characterized in the perichondrium around the condyle, whereas RARγ mRNA was expressed in the immature and prehypertrophic chondrocytes and the expression was overlapped with Ihh gene expression. Next we established a high-density culture model of chick cephalic chondrocytes in the prehypertrophic stage. We found that all-trans retinoic acid (RA) induced Ihh mRNA gene expression in this system. The RA pan-antagonist Ro 41-5253 inhibited both endogenous and RA-induced Ihh mRNA in a dose-dependent manner. The Ihh mRNA expression induced by RA required de novo protein synthesis, and was mediated by RARγ. Immunoblots showed that the prehypertrophic chondrocytes contained sizable levels of phosphorylated p38 mitogen-activated protein (MAP) kinase that were time- and dose-dependently increased by the RA treatment. Experimental p38 inhibition led to a severe drop in baseline and RA-stimulated Ihh expression. Exogenous recombinant Ihh stimulated the proliferation of proliferating chondrocytes, whereas RA inhibited the proliferation of these chondrocytes through p38 MAPK. Retinoids appear to play a primary role in controlling both the expression and function of Ihh in prehypertrophic chondrocytes and do so via p38 MAP kinase.