Arthritis Chronicle

A recent article in by Ehling and colleagues in the Journal of immunology looked into the potential that adiponectin has in driving arthritis.

Little is known about the local functions of articular adipose tissue (a ubiquitous component in human joints). Many recent publications have put forward possible links between adipocytokines, adipose tissue and arthritis. Ehling and friends looked at the ‘the adipocytokine adiponectin and its functional role in articular adipose tissue and synovium of patients with different arthritides’.

They found that ‘in contrast to its protective role in endocrinological and vascular diseases, adiponectin was found to be involved in key pathways of inflammation and matrix degradation in the human joint’

and that ‘ the effects of adiponectin in human synovial fibroblasts appear to be highly selective by inducing only two of the main mediators of rheumatoid arthritis pathophysiology, IL-6 and matrix metalloproteinase-1, via the p38 MAPK pathway’.

This led them to suggest that adipocytokines may be key targets in future therapeutic strategies in inflammatory joint diseases.

The full article is availble form pubmed PMID: 16547285 [PubMed - in process]

Bookmark to:

One of the consequences of infections of native joints is the development of suppurative arthritis. It is estimated that between two and five people in every hundred thousand of the general public will develop septic arthritis, this increases to around 35 people per hundred thousand in rheumatoid arthritis sufferers and to as high as 68 people in people who suffer from joint prostheses. Some of the events that precede this trauma include intravenous drug use and std’s, HIV, and diabetes. Skin infections are also often a cause of suppurative septic arthritis.

Staphylococcus aureus, may causes acute septic bursitis in up to 77% of cases. This usually occurs at the olecranon and pre-patellar bursea. Bacterial arthritis is also a common problem that leads to septic arthritis.

Chronic arthritis of joints is often a consequence of being infected by fungi. Some of the fungi that can cause chronic arthritis include Sporothrix schenckii (elbow, knee, wrist,) and Coccidioides immitis (knee, especially in americans). Following a trauma of the knee or elbow Pseudallescheria boydii may cause septic arthritis in tropical areas.

Bookmark to:

I stumbled on this intersting on cervical ankylosis effects, the study looked into the effects of mutation of the E250Q mutation found on the CD2BP1 gene, and discusses the variability of the results seen.

Here is the abstract of the article, I have given a link to the full text furter down the page

Objectives. To describe a family from New Zealand with the pyogenic arthritis, pyoderma gangrenosum and acne (PAPA) syndrome, an autoinflammatory, variably expressed, erosive destructive form of arthritis. 

So it’s a very small scale experiment

Methods. Information was gained through medical records and interviews of the affected patients and wider family. DNA sequencing was performed at Seay Center for Musculoskeletal Research Texas Scottish Rite Hospital for Children.

Simple well known procedures were used

Results. Five patients were affected over three generations with an E250Q mutation found on the CD2BP1 gene on chromosome 15. Common features included a severe, pauciarticular-onset, destructive peripheral arthritis, beginning at ages 5, 5, 2, 3 and 1 years. This combination marked cervical ankylosis (in two members), micrognathia and a more severe phenotype is unique. A third-generation family member treated early with DMARDs is following a less severe course. The skin involvement was variable, all with degrees of acne from puberty, though only one patient displayed pyoderma gangrenosum. A clear pattern of the arthritis switching off in adolescence and the triggering of skin disease was observed.

So it seems that different members of the family with the same gene defect have varying levels of pain

Conclusions. Differing degrees of joint destruction, and cervical ankylosis in this family with the E250Q mutation demonstrate PAPA syndrome’s variable expression. Further understanding of this rare condition and its pathway may allow better targeting of treatments, not just for families with this specific syndrome but also for other, more common, forms of arthritis.

Unfortunately io could not get full access to this article so am unable to give it a full scale review! for those who may have access through a university, heres a link to the cervical ankylosis article 

Full article is available from Rheumatology

 http://rheumatology.oxfordjournals.org/cgi/content/abstract/kei178v1

Bookmark to: