Study Design Case report and review of the literature. Objective A retro-odontoid mass is a rare cause of cervical compression and myelopathy. The differential diagnosis includes the following: metastatic disease, primary tumor, collagen disorder, or inflammatory disease. Calcium pyrophosphate dihydrate (CPPD) deposition has been referred to as “crowned dens syndrome” when there are periodontoideal calcifications. There are only a few reported cases where CPPD presents as a cystic retro-odontoid mass in the atlanto-dens interval. In previous descriptions of surgical intervention, transoral resection of the mass is associated with significant morbidity and usually requires stabilization. The objective of this article is to report a case of an unusual presentation of CPPD disease of C1/C2, where we used a novel, minimally invasive surgical technique for decompression without fusion. Patients and Methods An 83-year-old female patient presented with progressive cervical myelopathy over a 3-month period. Computed tomography and magnetic resonance imaging demonstrated a cystic odontoid mass with a separate retro-odontoid compressive mass. A novel, minimally invasive transoral aspiration was performed. Histologic confirmation of CPPD was obtained. Results Postop imaging showed satisfactory decompression, which was maintained at the 6-month follow-up. This correlated with clinical improvement postop and 6-month follow-up. Conclusion CPPD in the atlanto-dens interval may present as a cystic retro-odontoideal mass and should be included in the differential. We used a transoral minimally invasive approach to aspirate the cyst. This novel technique avoided the need for a stabilization procedure or morbid transoral resection and provided excellent results immediately and at 6 months.

Biomimetic proteoglycans (BPGs) have the potential to treat osteoarthritis (OA) given that these molecules mimic the structure and properties of natural proteoglycans, which are significantly reduced in OA. We examined the effects of BPGs injected into the intra-articular space in an in vivo OA rabbit knee model and evaluated the effect on histological response, joint friction, and BPG distribution and retention. Rabbits underwent ACL transection to create an arthritic state after 5 weeks. OA rabbits were treated with BPGs or Euflexxa 1 (hyaluronic acid) intra-articular injections. Non-OA rabbits were injected similarly with BPGs; contralateral joints served as controls. The progression of OA and response to injections were evaluated using Mankin and gross grading systems indicating that mild OA was achieved in operated joints. The coefficient of friction (COF) of the intact knee joints were measured using a custom pendulum friction apparatus, showing that OA joints and OA þ Euflexxa 1 joints demonstrated increased COF than nonoperated controls, while BPG-injected non-OA and OA þ BPGs were not significantly different from non-OA controls. Injected fluorescently labeled BPGs demonstrated that BPGs diffused into cartilage with localization in the pericellular region. ß

The results of light and electron microscopic examination and of biochemical proteoglycan studies of costochondral and iliac crest biopsies from a recently diagnosed case of Dyggve-Melchior-Clausen dysplasia are reported. At light microscopy of resting cartilage large lacunae containing clusters of five or more chondrocytes were seen in some areas. In the hyaline cartilage there were scattered fibrous foci but no mineralized areas. Electron microscopy revealed chondrocytes containing widened cisternae of rough endoplasmic reticulum and vesicles coated with a smooth single-layered membrane. The content of the cisternae and of the vesicles was amorphous. Throughout the cartilage a considerable proportion of the chondrocytes displayed more or less pronounced necrobiotic changes. The biochemical analysis showed an increased amount of glucosaminoglycans in the cartilage and indicated that the ability of proteoglycan monomers to reaggregate to hyaluronic acid chains was decreased. Our findings support the suggestion that Dyggve-Melchior-Clausen dysplasia is due to a disturbance in proteoglycan metabolism.