Arthritis is CAUSED in this animal model by using iron to induce
oxidation.
------------------------

Free radical damage in facsimile synovium: correlation with adhesion
formation in osteoarthritic TMJs.
Sheets DW, Okamoto T, Dijkgraaf LC, Milam SB, Schmitz JP, Zardeneta G
J Prosthodont. 2006 Jan-Feb ; 15(1): 9-19

PURPOSE: The purpose of this study was to use the rat air pouch model
of facsimile synovium to evaluate oxidative stress as a primary
mechanism in the pathogenesis of degenerative temporomandibular joint
(TMJ) disease. MATERIALS AND METHODS: Forty-nine Sprague-Dawley adult
female rats were used to generate the standard rat air pouch model of
facsimile synovium. This was accomplished by daily air injections (20
cc) subdermally through the dorsal skin. Hydrogen peroxide and ferrous
iron (components of the Fenton reaction which generate free radicals)
were introduced into the pouches of the 4-, 7-, and 14-day groups to
generate oxidative stress. Control rats were injected with
phosphate-buffered solution (PBS), pH 7.4. Either N-acetylcysteine
(NAC), a powerful free radical scavenger, or ibuprofen were
simultaneously injected with the Fenton reagents into the pouches of
the 14-day treatment groups to modulate free radical-mediated protein
damage to the synovium. Animals were euthanized at appropriate
experimental intervals and biopsies obtained from specimens to analyze:
(1) proteins' amino acid modification (carbonyl group formation), (2)
protein hydrophobicity, (3) detection of low molecular weight protein
degradation products, and (4) histological and gross anatomical
observations. RESULTS: Free radicals introduced into the rat air pouch
interacted with synovial tissues causing oxidation and breakdown of
proteins. Clinical evidence of adhesion formation consistent with
features found in osteoarthritis of the TMJ developed. The groups
subjected to oxidative stress experienced statistically significant (p
< 0.05) increases in carbonyl formation, carbonyls/protein, and low
molecular weight protein fragments. These groups also showed
significant (p < 0.05) hydrophobicity changes consistent with free
radical attack. Control synovial tissues were statistically undamaged.
The 14-day NAC and ibuprofen treatment groups experienced statistically
significant (p < 0.05) decreases in total carbonyl formation,
carbonyls/protein, and hydrophobicity. Histological and gross
observations in free radical damaged synovium exhibited features
consistent with known arthoscopic and arthrocentesis findings in
diseased TMJs. Conclusions: This study suggests that the rat air pouch
model of facsimile synovium develops clinical evidence of adhesions and
biochemical signs of protein modification when subjected to free
radical attack. NAC and ibuprofen prevented carbonyl formation as well
as hydrophobicity changes indicative of oxidative stress damage in
facsimile synovium. These findings are consistent with features of
degenerative human TMJ disease. Future direction may be taken from this
study to postulate new analysis techniques and treatment modalities for
patients with degenerative TMJ disease.

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