Case Report: Vision Loss in a Child Caused by Streptococcus constellatus.

PURPOSE: We present a rare case of Streptococcus constellatus -induced odontogenic orbital cellulitis. METHODS: An 8-year-old boy presented to an outpatient clinic with complaints of right-sided toothache, right eye swelling, and decreased visual acuity. He was referred to a pediatric critical care department for further management. Comprehensive diagnostic assessments, such as ophthalmic examination, blood tests, computed tomography, and MRI, were performed. RESULTS: On presentation, the best-corrected visual acuities were 20/250 and 20/20 in the right and left eyes, respectively. Examination revealed grade 2+ eyelid edema and erythema and grade 4+ chemosis and exophthalmos in the right eye. The patient displayed restricted eye movements in all directions. Blood tests revealed a total white blood cell count of 12,100 cells/µL. Axial and coronal computed tomography revealed right-sided maxillary sinus, ethmoidal sinus, and orbital abscesses. Therefore, the patient was diagnosed with septicemia, orbital cellulitis, and orbital apex syndrome in the right eye. Intravenous antibiotics were administered; paracentesis of the orbital abscess was performed under local anesthesia. However, the patient's condition worsened, resulting in a complete loss of light perception in the right eye. Accordingly, surgery was performed under general anesthesia within 24 hours of admission; the surgery involved drainage of the orbital abscess through an inferior intraorbital incision, as well as drainage of the ethmoid sinus and maxillary sinus abscesses via nasal endoscopy. A culture obtained from the orbital abscess yielded S. constellatus . The infection was managed by a combination of surgical intervention, antibiotics, steroids, and hyperbaric oxygen therapy. However, because of optic nerve injury, vision in the affected eye partially recovered to 20/200. CONCLUSIONS: Streptococcus constellatus -induced pediatric orbital cellulitis can result in significant morbidity. The significant improvement in vision, from no light perception to 20/200, emphasizes the importance of timely diagnosis and treatment in patients who present with acute orbital cellulitis and vision loss symptoms.

Folate ameliorates homocysteine-induced osteoblast dysfunction by reducing endoplasmic reticulum stress-activated PERK/ATF-4/CHOP pathway in MC3T3-E1 cells.

INTRODUCTION: Homocysteine (Hcy) is considered a newly identified risk factor for osteoporosis. Nevertheless, the underlying mechanism of folate (FA), a key factor in the metabolism of Hcy, in protection against osteoblast dysfunction remains unclear. The purpose of this study was to investigate the mechanism by which FA attenuates Hcy-induced osteoblast damage. MATERIALS AND METHODS: The Hcy-induced MC3T3-E1 cells were treated with different concentrations of FA. Cell morphology, cell density, cell proliferation ability, alkaline phosphatase (ALP) activity and mineralization capacity were observed and determined; the gene expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (BAX) and ERS-associated factors, including glucose-regulated protein 78 (GRP-78), activating transcription factor 4 (ATF-4) and growth arrest and DNA damage inducible gene 153 (CHOP/GADD153), were assessed by RT-PCR; and protein levels of GRP-78 and ATF-4 were analyzed by western blotting. RESULTS: Hcy suppressed the proliferation, differentiation and mineralization ability of MC3T3-E1 cells in a concentration-dependent manner and activated the ERS signaling pathway. After intervention with different concentrations of FA, the cell viability and density, ALP activity, number of mineralized nodules, calcium content and Bcl-2 gene expression were all significantly increased, whereas the gene expression of GRP-78, CHOP/GADD153, ATF-4 and Bax was markedly downregulated, and protein levels of GRP-78 and ATF-4 were also markedly decreased. CONCLUSION: The adverse effects of Hcy on osteoblast differentiation are dose dependent. FA not only protects against osteoblasts apoptosis but also has a direct osteogenic effect on Hcy-induced osteoblasts, which could be partially mediated by inhibition of the PERK-activated ERS pathway.