PubMed Health⌕ Search

PubMed · 12567134

Milwaukee shoulder: correlating possible etiologic variables.

Abstract

The current study evaluated the relative correlation of apatite crystal-induced inflammation and rotator cuff deficiency in the development of cuff tear arthropathy. Thirty-seven patients with full thickness rotator cuff tears were evaluated by history, physical examination, and plain radiographs. Thirty patients had surgical intervention for their rotator cuff defects, and calipers were used intraoperatively to quantify the size of the tear in its largest diameter. The remaining seven patients were treated nonoperatively and the size of the tear was quantified using magnetic resonance imaging. Synovial fluid was obtained from all patients and analyzed for crystal content using an alizarin red stain. Synovial fluid also was analyzed for leukocyte count and differential, prostaglandin E, and matrix metalloproteinase. An unpaired Student's t test revealed that significantly higher levels of prostaglandin E were found in the synovial fluid of patients with apatite crystals, shown by alizarin red stain. Chi squared analysis showed that patients with elevated crystal levels were significantly more likely to have large rotator cuff tears or glenohumeral arthritis. Establishing such relations potentially can elucidate the etiology and treatment of this complex disorder.(2) (2)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

John Antoniou, Albert Tsai, Dan Baker, Ralph Schumacher, Gerald R Williams, Joseph P Iannotti. 2003. Milwaukee shoulder: correlating possible etiologic variables.. https://doi.org/10.1097/00003086-200302000-00015

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Interleukin-18 genetics and inflammatory disease susceptibility.

IL18 was mapped to 11q22.2-22.3 in 1998. Owing to interleukin (IL)-18's important and novel role in immunomodulation, the gene itself has been subject to scrutiny, with the aim of discovering variants that may impact on disease susceptibility and/or progression. Despite being sequenced numerous times in different populations, no non-synonymous variants have been found. However, a number of polymorphisms within the proximal promoter have been verified that may interfere with transcription-factor-binding sites. Much of the subsequent association analyses have centred on these variants, but have yielded no consistent results, despite numerous different study populations being genotyped. IL18 has recently been resequenced in its entirety, enabling the tagging-single-nucleotide polymorphism (tSNP) methodology to be adopted. This approach has yielded interesting results, with genetic variation being shown to affect protein levels, and risk. This review aims to compile and reflect on the association data of interest published to date, with a focus on the diseases related to aberrant inflammatory control.

Arthritis↗