On Jan 29, 10:13 am, numbnutz again spewed:

Created with  CANINE TEETH  to bite and chew  MEAT.

... numbnutz tom always hits the nail right on the thumb.

On Jan 29, 10:13 am, numbnutz "ironjust" posted before reading:

Created with CANINE TEETH to rip, chew, and eat meat.

Scares the $hit out of numbnutz tom.

... numbnutz tom gets change back when he posts his 2 cents.

<snip>

Tom, what's *your* definition of "spillage" as you used it here?

He couldn't find a document MORE RECENT than *1980*
to cite the causes of OA??  Nobody's looked into it since then?  ;-)

Oy.

Ginnie &  >^..^<
__________________________

What ARE you talking about?

His mother kept him in a cage...

Has he landed again...I would never know unless someone responds...as I
killfiled for good...good thing some of you are out there to warn the
unknowing and naive ones from the pscyho nut...

On Jan 28, 1:19 pm, Steven <s...@msn.com> wrote:

Someone once said on this site that osteo starts with inflammation. I
subscribe to that theory. Something has to set off the wear and tear.
The things that are wrong with me are all related to arthritis-- both
hips replaced, an inflammatory bowel disease, with accompanying eye
involvement, and rosacea. I just wonder if there is some way to stop
the inflammation before it starts. Although it's too late for me and
loads of other people it would be a worthwhile thing to study since
arthritis is so prevalent.

i'm one who subscribes to inflammation being the most destructive influence,
but i think irritation is at least one initiator of joint inflammation.  but
then, i don't know much.

kate

These articles suggest that since we know that MMPs does the actual damage
in arthritis that
reducing them a tad might help. They specialize in cutting things up with
their Zinc ion tips. They
mistakenly cut up worn cartilage that cannot be easily replaced.

What causes this unwanted excessive MMP activity is unknown.

I have found that a number common meds and supplements (especially certain
families of flavonoids) have been shown to reduce these specific
MMPs involved in arthritis.(MMP-1, MMP-2, MMP-3, MMP-9, MMP-13)

Taking the correct ones to reduce a specific MMPs should be quite harmless
and helpful. I can elaborate on this if requested. Checking PubMed (NLM) on
MMPs and arthritis would be a good idea.

http://www.pubmed.gov

jack n dalton

P.S. I have posted this before but since no one seems  understand or care
about this approach I will just say  "Here it is again ..folks!!!"

Ann Anat. 2005 Nov;187(5-6):473-85. Related Articles, Links

Pathomechanisms of cartilage destruction by mechanical injury.

Kurz B, Lemke AK, Fay J, Pufe T, Grodzinsky AJ, Schunke M.

Anatomisches Institut der Christian-Albrechts-Universitat zu Kiel,
Olshausenstrasse 40, D-24098, Kiel, Germany

Mechanical injury is considered to be a major inductor of articular
cartilage destruction and therefore a risk factor for the development of
secondary osteoarthritis. Mechanical injury induces damage to the tissue
matrix directly or mediated by chondrocytes via expression of
matrix-degrading enzymes and reduction of biosynthetic activity. As a
consequence the mechanical properties of cartilage change. Some of the
pathomechanisms of mechanical injury have already been uncovered by the use
of a broad range of in vitro-models. They demonstrate that mechanical injury
induces tissue swelling and decrease in both the compressive and shear
stiffness of articular cartilage, probably due to disruption of the collagen
network. Injurious compression induces chondrocyte death by necrosis and
apoptosis and the remaining cells decrease their biosynthetic activity. The
tissue content of proteoglycans also decreases with time in injured
cartilage, and the tissue loses its ability to respond to physiological
levels of mechanical stimulation with an increase in biosynthesis. Immature
cartilage seems to be more vulnerable to injurious compression than more
mature tissue. The expression of several matrix-degrading enzymes like
ADAM-TS5 and matrix-metalloproteinases (MMP-1, MMP-2, MMP-3, MMP-9, MMP-13)
is increased after injury and may in part be regulated by an autocrine
vascular endothelial growth factor (VEGF)-dependent signalling pathway.
Apoptosis seems to be mediated by caspase activity and reactive oxygen
species.

For that reason activation of antioxidative defense mechanisms as
well as the inhibition of angiogenetic factors and MMPs might be key
regulators in the mechanically induced destruction of cartilage and might be
suggested as potential therapeutic interventions. This review summarizes
some of the most important data from in vitro injury studies dealing with
the pathomechanisms of cartilage destruction.

Publication Types:
 a.. Review

PMID: 16320827 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16146751&query_hl=7&itool=pubmed_docsum
...
...
Front Biosci. 2006 Jan 1;11:529-43. Related Articles, Links

Matrix metalloproteinases: role in arthritis.

Burrage PS, Mix KS, Brinckerhoff CE.

Department of Biochemistry, Dartmouth Medical School, Dartmouth Hitchcock
Medical Center, Lebanon, NH 03756, USA.

The irreversible destruction of the cartilage, tendon, and bone that
comprise synovial joints is the hallmark of both rheumatoid arthritis (RA)
and osteoarthritis (OA). While cartilage is made up of proteoglycans and
type II collagen, tendon and bone are composed primarily of type I collagen.
RA is an autoimmune disease afflicting numerous joints throughout the body;
in contrast, OA develops in a small number of joints, usually resulting from
chronic overuse or injury.

In both diseases, inflammatory cytokines such as
interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha)
stimulate the production of matrix metalloproteinases (MMPs), enzymes that
can degrade all components of the extracellular matrix.

The collagenases,
MMP-1 and MMP-13, have predominant roles in RA and OA because they are rate
limiting in the process of collagen degradation. MMP-1 is produced primarily
by the synovial cells that line the joints, and MMP-13 is a product of the
chondrocytes that reside in the cartilage.

In addition to collagen, MMP-13 also degrades the proteoglycan molecule,
aggrecan, giving it a dual role in
matrix destruction. Expression of other MMPs such as MMP-2, MMP-3 and MMP-9,
is also elevated in arthritis and these enzymes degrade non-collagen matrix
components of the joints.

Significant effort has been expended in attempts
to design effective inhibitors of MMP activity and/or synthesis with the
goal of curbing connective tissues destruction within the joints. To date,
however, no effective clinical inhibitors exist. Increasing our knowledge of
the crystal structures of these enzymes and of the signal transduction
pathways and molecular mechanisms that control MMP gene expression may
provide new opportunities for the development of therapeutics to prevent the
joint destruction seen in arthritis.

PMID: 16146751 [PubMed - in process]