BACKGROUND Crowned dens syndrome (CDS) is a rare disorder caused by calcium pyrophosphate deposition around the odontoid process. Although most patients respond favorably to conservative management, some develop refractory myelopathy requiring surgical intervention. We present a minimally invasive surgical technique for CDS complicated by spinal cord compression. CASE REPORT An 86-year-old woman with CDS exhibited progressive myelopathy, including thoracoabdominal girdle sensation, gait disturbance ("walking on cotton"), and impaired fine motor function in the upper extremities. Her symptoms were refractory to 9 months of conservative treatment. Computed tomography and magnetic resonance imaging demonstrated calcification of the transverse and alar ligaments at the craniovertebral junction with associated compression of the medulla oblongata. The patient underwent unilateral biportal endoscopic resection of the posterior arch of the atlas with spinal canal decompression. Intraoperatively, a midline bony defect was identified. Approximately 8 mm of the posterior arch was resected bilaterally using a high-speed drill; partial excision of the posterior atlanto-occipital membrane and posterior atlantoaxial ligament was performed. Postoperatively, neck pain and girdle sensation were greatly alleviated. At the 1-year follow-up, gait stability and fine motor function had substantially improved, the Japanese Orthopaedic Association score increased from 9 to 12, and no procedure-related complications were observed. CONCLUSIONS Unilateral biportal endoscopic posterior arch resection of the atlas with decompression represents a feasible and minimally invasive alternative to conventional open surgery for selected patients with CDS displaying myelopathy, particularly high-risk older individuals. This case underscores the importance of surgical intervention in patients with CDS and spinal cord compression.

Colchicine is an ancient drug that remains a cornerstone in the management of crystal-induced inflammatory diseases, particularly gout and calcium pyrophosphate crystal disease (CPPD). Its clinical use is supported by well-established pharmacological and mechanistic evidences, mainly derived from experimental studies. Colchicine interferes with microtubule-dependent cellular functions, inhibits neutrophil activation, and modulates NLRP3 inflammasome signalling, resulting in reduced interleukin-1β production. In addition, colchicine exerts pleiotropic anti-inflammatory effects that extend beyond crystal synovitis, including modulation of platelet-leukocyte interactions and vascular inflammation. Owing to its narrow therapeutic index, low-dose regimens and careful attention to drug-drug interactions are essential. This narrative review summarises the pharmacology, mechanisms of action, and clinical applications of colchicine in rheumatic disorders, particularly gout and CPPD, and its expanding use in cardiovascular diseases, dermatology, and other inflammatory disorders.

Definitive diagnosis of gout relies on the identification of monosodium urate (MSU) crystals in synovial fluid. This process has confounders, including differentiating different crystal types, which require a high level of skill and relevant equipment. The Royal College of Pathologists of Australasia Quality Assurance Programs has provided a synovial fluid crystal identification external quality assurance (EQA) program for 15 years. In this article, we describe and analyse the current and past performance of this program. The key findings are that synovial fluid crystal identification has been and remains suboptimal in a significant proportion of the program's laboratories. There are consistently poorly performing laboratories, and there is a general issue with differentiating between MSU and calcium pyrophosphate crystals. The identification of MSU crystals provides definitive diagnosis of gout, leading to a lifetime treatment. Therefore, this represents an area of laboratory practice where more training is required to reduce patient risk.