11 research outputs found

    Skin pentosidine in very early hip/knee osteoarthritis (CHECK) is not a strong independent predictor of radiographic progression over 5 years follow-up

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    SummaryObjectivesAge-related changes in articular cartilage are likely to play a role in the etiology of osteoarthritis (OA). One of the major age-related changes in cartilage is the accumulation of advanced glycation end products (AGEs). The present study evaluates whether pentosidine can predict radiographic progression and/or burden over 5 years follow-up in a cohort of early knee and/or hip OA.DesignThe 5 years follow-up data of 300 patients from cohort hip & cohort knee (CHECK) were used. Radiographic progression and burden were assessed by X-rays of both knees and hips (Kellgren and Lawrence (K&L) and Altman scores). Baseline pentosidine levels (and urinary CTXII as a comparator) were measured by high-performance-liquid-chromatography (HPLC) and enzyme linked immunosorbent assay (ELISA). Univariable and multivariable associations including baseline radiographic damage, age, gender, body mass index (BMI) and kidney function were performed.ResultsBoth pentosidine and urinary C-terminal telopeptide of type II collagen (uCTXII) correlated with radiographic progression and burden. In general pentosidine did not have an added predictive value to uCTXII for progression nor burden of the disease. The best prediction was obtained for burden of radiographic damage (R2 = 0.60–0.88), bus this was predominantly determined by baseline radiographic damage (without this parameter R2 = 0.07–0.17). Interestingly, pentosidine significantly added to prediction of osteophyte formation, whereas uCTXII significantly added to prediction of JSN in multivariable analysis.ConclusionPentosidine adds to prediction of radiographic progression and burden of osteophyte formation and uCTXII to radiographic progression and burden of JSN, but overall skin pentosidine did not perform better that uCTXII in predicting radiographic progression or burden. Burden of damage over 5 years is mainly determined by radiographic joint damage at baseline

    Cervical myelopathy caused by soft-tissue mass in diffuse idiopathic skeletal hyperostosis

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    A rare case of cervical spinal cord compression in diffuse idiopathic skeletal hyperostosis (DISH or Forestier’s Disease) caused by a craniocervical mass of soft-tissue is reported. The objective is to describe an uncommon mechanism of spinal cord compression in DISH. Three weeks after a cardiac infarction a 69-year-old man slowly developed spastic tetraparesis. Magnetic resonance tomography showed a craniocervical tumor compressing the spinal cord and a massive DISH of the cervical spine. An extended mass of yellowish amorphous material was removed from between the dura, the posterior odontoid process and the posterior aspect of vertebral body C2 reaching to the upper part of C3.The histologic appearance indicated connective tissue and cell-degenerated cartilaginous tissue. There was no inflammatory component and no evidence of neoplasia. No ossification of the posterior longitudinal ligament (OPLL) was found. After removal and craniocervical stabilization the patient’s neurologic function improved remarkably. The increase of mechanical stress on the atlantoaxial segment and enhanced proliferation reaction of the connective tissue in DISH are suggested as the underlying pathomechanisms in the formation of this soft-tissue mass
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