If the ingestion of different fatty acids changes the fatty acids in
the mammals body would the ingestion and / or liberal application of
topical lecithin BE an effective alternative to these injections.. ?
Lecithin bathes the joints / lubricant.

--------------------------------------------
Lack Of Critical Lubricant Causes Wear In Joints, First-Ever Study
Finds
Main Category: Arthritis News
Article Date: 07 Nov 2007 - 1:00 PST

Mice that don't produce lubricin, a thin film of protein found in the
cartilage of joints, showed early wear and higher friction in their
joints, a new study led by Brown University researchers shows.

This link between increased friction and early wear in joints is a
first; no other team of scientists has proven this association before.
The finding, published in Arthritis & Rheumatism, sheds important
light on how joints work. The discovery also suggests that lubricin,
or a close cousin, could be injected directly into hips, knees or
other joints inflamed from arthritis or injury -- a preventive
treatment that could reduce the need for painful and costly joint
replacement surgery.

In an editorial that accompanies the journal article, orthopedics
researchers from Rush University Medical Center in Chicago call the
research an "important contribution to the field" and note that the
use of biomolecules like lubricin to prevent joint wear "could have a
substantial clinical impact, if successful."

Gregory Jay, M.D, a Rhode Island Hospital emergency physician and an
associate professor of emergency medicine and engineering at Brown,
led the research. For 20 years, Jay has studied lubricin's role as a
"boundary lubricant" by reducing friction between opposing layers of
cartilage inside joints. In this new work, Jay and his colleagues set
out to answer the next question: Does reducing friction actually
prevent wear, or surface damage, in joints?

To find out, Jay and his team studied cartilage from the knees of mice
that don't produce lubricin. Directly after birth, the cartilage was
smooth. But in as little as two weeks, researchers found, the
cartilage began to show signs of wear. Under an electron microscope,
scientists could see that the collagen fibers that cartilage is
composed of were breaking up, giving the surface a rough, frayed
appearance. This damage is called wear, an early sign of joint disease
or injury.

Jay and his team then took the work a step further. To better
understand how lubricin works, they tried to see the structure of the
film. So they put a tiny bit of the protein under an atomic force
microscope. At the nanoscale, the molecule appeared as a mesh -- row
upon row of interlocking fibers -- that could repel a microscope
probe. This repulsion, created with water and electrical charges,
shows how lubricin acts as a buffer, keeping opposing layers of
cartilage apart.

"We demonstrated that lubricin reduces both friction and wear and also
showed how, on a molecular level, it does this work in the body," Jay
said. "What's exciting are the clinical implications. Arthritis and
sports injuries damage the joints of thousands of people in the United
States and millions of people worldwide each year. Our aim is to make
a treatment that can actually prevent wear in the joints."

Through Rhode Island Hospital, Jay has filed two patents on the
protein and its sequences and, in 2004, helped form Tribologics, a
biotech company formed out of Rhode Island Hospital. The
Massaschusetts-based business is developing an injection treatment for
inflamed joints that contains lubricin.

Members of the research team included Jahn Torres, a former Brown
graduate student in engineering; David Rhee, a former graduate student
at Case Western Reserve University; Heikki Helminen, M.D., and Mika
Hytinnen, M.D., from the University of Kuopio in Finland; Chung-Ja
Cha, a research assistant at Rhode Island Hospital; Khaled Elsaid, a
postdoctoral research fellow at Rhode Island Hospital; Kyung-Suk Kim,
a professor of engineering at Brown; and Yajun Cui, M.D., and Matthew
Warman, M.D., of Boston Children's Hospital and Harvard Medical
School.

The National Institute of Arthritis and Musculoskelatal and Skin
Diseases funded the work, along with the Academy of Finland, the
McCutchen Foundation, the Howard Hughes Medical Institute and the
Burroughs Wellcome Fund.

Source: Wendy Lawton
Brown University

--------------------------------------------------

J Orthop Surg. 2007 Aug 23;2(1):14 [Epub ahead of print] Links
Unsaturated phosphatidylcholines lining on the surface of cartilage
and its possible physiological roles.
Chen Y, Crawford RW, Oloyede A.
ABSTRACT:
BACKGROUND:
Evidence has strongly indicated that surface-active phospholipid
(SAPL), or surfactant, lines the surface of cartilage and serves as a
lubricating agent. Previous clinical study showed that a saturated
phosphatidylcholine (SPC), dipalmitoyl-phosphatidylcholine (DPPC),
was
effective in the treatment of osteoarthritis, however recent studies
suggested that the dominant SAPL species at some sites outside the
lung are not SPC, rather, are unsaturated phosphatidylcholine (USPC).
Some of these USPC have been proven to be good boundary lubricants by
our previous study, implicating their possible important
physiological
roles in joint if their existence can be confirmed. So far, no study
has been conducted to identify the whole molecule species of
different
phosphatidylcholine (PC) classes on the surface of cartilage. In this
study we identified the dominant PC molecule species on the surface
of
cartilage. We also confirmed that some of these PC species possess a
property of semipermeability.
METHODS:
HPLC was used to analyse the PC profile of bovine cartilage samples
and comparisons of DPPC and USPC were carried out through
semipermeability tests.
RESULTS:
It was confirmed that USPC are the dominant SAPL species on the
surface of cartilage. In particular, they are Dilinoleoyl-
phosphatidylcholine (DLPC), Palmitoyl-linoleoyl-phosphatidylcholine,
(PLPC), Palmitoyl-oleoyl-phosphatidylcholine (POPC) and Stearoyl-
linoleoyl-phosphatidylcholine (SLPC). The relative content of DPPC (a
SPC) was only 8%. Two USPC, PLPC and POPC, were capable of generating
osmotic pressure that is equivalent to that by DPPC.
CONCLUSIONS:
The results from the current study confirm vigorously that USPC is
the
endogenous species inside the joint as against DPPC thereby
confirming
once again that USPC, and not SPC, characterizes the PC species
distribution at non-lung sites of the body. USPC not only has better
anti-friction and lubrication properties than DPPC, they also possess
a level of semipermeability that is equivalent to DPPC. We therefore
hypothesize that USPC can constitute a possible addition or
alternative to the current commercially available
viscosupplementation
products for the prevention and treatment of osteoarthritis in the
future.

PMID: 17718898 [PubMed - as supplied by publisher]

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