BackgroundIt’s difficult to diagnose and treat synovitis-acne-pustulosis-hyperostosis-osteomyelitis (SAPHO) syndrome due to its rare and unknown pathogenesis. There is no effective treatment for SAPHO syndrome and the consequences of empirical treatment are unpredictable. This study reports a case of a young female diagnosed as SAPHO syndrome with pathological fractures of vertebral bodies.Case presentationA 29-year-old female complained of the right sternoclavicular joint and back pain accompanied limited activities and cutaneous lesions. Laboratory assays revealed abnormal inflammatory factors. Multiple imaging studies illustrated bone lesions and pathological fractures of vertebral bodies. A diagnosis of SAPHO syndrome was made. The patient was treated with Compound Troxerutin and Poreine Cerebroside Injection, non-steroidal anti-inflammatory drugs (NSAIDs), bisphosphonates, corticosteroids and the thoracolumbar brace. The patient was followed up for 6 months and showed improved results.ConclusionsThe case supports that multiple image inspections and laboratory tests contribute to diagnose SAPHO syndrome, and combination therapies of Compound Troxerutin and Poreine Cerebroside Injection, NSAIDs, bisphosphonates, corticosteroids and the thoracolumbar brace in the treatment of SAPHO syndrome with pathological fractures of vertebral bodies are crucial to regain health.

BackgroundOral squamous cell carcinoma (OSCC) ranks as the fifth most frequent cancer worldwide, and the recurrence and migration of OSCC still pose large threats to patients. Long non‐coding RNAs (lncRNAs) have recently emerged as crucial players in cancer development, and it is of great significance to understand the regulatory nexus of lncRNAs in OSCC.MethodsHere, we identified a novel lncRNA, RP11‐874J12.4, which is ectopically expressed in OSCC and facilitates OSCC.ResultsRP11‐874J12.4 directly binds to and regulates miR‐19a‐5p. Interestingly, RP11‐874J12.4 and miR‐19a‐5p form a negative regulatory loop that inhibits the expression of miR‐19a‐5p in OSCC. The expression of an oncogenic transcription factor, EBF1, is unleashed in OSCC due to the low expression of miR‐19a‐5p, which promotes the growth and migration of OSCC.ConclusionOur data illustrate a regulatory axis of RP11‐874J12.4/miR‐19a‐5P/EBF1 and an inhibitory loop with RP11‐874J12.4 and miR‐19a‐5p. These data provide insights into the tumorigenesis of OSCC and the novel drug targets for OSCC.