Quelae in the locomotor and/ or cardiovascular system are not fully understood, but with modern targeted therapies and translational in vitro research we are starting to unravel these processes. With this information, and if pharmacotherapeutic options are administered appropriately, we, as clinicians, should be able to solve the devilish problems of ancient `gutta’. Gutta is the origin of the word gout, the Latin word for a*Correspondence: [email protected] Department of Rheumatology, Radboud University Nijmegen Medical Centre, Geert Grooteplein Noord 10, 6525 GA Nijmegen, The Netherlands?2010 BioMed Central Ltd?2012 BioMed Central LtdJansen Arthritis Research Therapy 2012, 14:126 http://arthritis-research.com/content/14/6/Page 2 ofFigure 1. Schematic presentation of gout etiopathogenesis with the therapeutic arsenal for the clinician. The asterisk indicates that these are in development. NSAID, non-steroidal anti-inflammatory drug; PNPi, purine nucleotide phosphorylase inhibitor; XOI, xanthine oxidase inhibitor.of the proinflammatory cytokine TNF and the TNFinducible lytic enzymes MMP-2 and MMP-9. MSU crystals (S)-(-)-Blebbistatin chemical information reduce the effects of anabolic osteoblasts, and seem to alter the normal balance between RANKL and osteoprotogerin, thereby indirectly promoting osteoclastogenesis in MSU-induced arthritis. IL-1 is a key molecule in TNF- and RANKL-induced osteoclastogenesis. The effects of the IL-1 receptor antagonist on markers of bone erosion and cartilage damage appear to be superior to its effects on inflammation, at least in rheumatoid arthritis. Early detection and treatment of arthritic gout attacks have been prioritized over the past decades. Polarisation microscopy of the punctate (gold standard) and ultrasonography significantly contribute to early diagnosis in gout. Common radiology contributes to late gout diagnoses as it often takes years to develop radiographic abnormalities. In longstanding, often non-arthritic gout, tophaceous bulky disease may even coincide with common as well as more specific radiographic lesions. Dalbeth and colleagues [4] performed a quantitative analysis of radiography and tomography (798 joints photographed) in longstanding, often (80 ) tophaceous gout (20 patients with about 20 years of exposure to a serum urate of about 0.49 mmol/l), an interesting experimental setting indeed. Gout attacks are considered to result in soft tissue swelling, cartilage loss and periarticular osteopenia.Characteristic but not diagnostic for gout are radiographic features such as punched-out lytic lesions of articular bone [4], not to be confused with rheumatoid erosions. In gout these lytic lesions appear as sharp, often marginated lucent pockets, or discrete subchondral `pseudocysts’ seemingly not connected to the joint. Sclerotic margins signal bone repair in temporarily nonusurating foci. At the periphery of this `erosive’ lesion the bone margin appears to even hang over the tophaceous debris, particularly in hand/foot radiographs [5]. In the presented series about 30 of small hand joints were `erosive’ at radiography, and a similar percentage at tomography. These `erosive’ lesions differ from rheumatoid arthritis with respect to appearance and the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25962748 high frequency of occurrence in gout cases. Displacement of the margin probably reflects a gradual increase in size of the urate nidus, growing by multicentric deposition of urate crystals. In the vicinity of tophi, osteoblast activity is reduced and osteoclast activity.
