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(Anatomy) (Health) Joints: The Inflamed Synovium (Arthritis)

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PostPosted: Wed Mar 29, 2006 7:09 am    Post subject: (Anatomy) (Health) Joints: The Inflamed Synovium (Arthritis) Reply with quote

John Wiley & Sons, Inc.
29 March 2006

Targeting the inflamed synovium

Exploring the promise and imperative of tissue-specific strategies for the treatment of rheumatoid arthritis
Rheumatoid arthritis (RA) is a complex and destructive inflammatory disease. Despite recent impressive advances in disease-modifying antirheumatic drugs and biologic therapies, treatment is not always effective and still has many safety ramifications. Assessment of RA, once dependent on X-ray measurement of cartilage and bone destruction, has also experienced dramatic gains with the use of magnetic resonance imaging and ultrasound. Still, accurate early detection and monitoring of short-term changes in simultaneous joints remains elusive.
To further improve the delivery of both drugs and imaging agents for the treatment of RA, researchers are increasingly focusing on the inflamed tissue that leads to joint destruction¡Xthe synovium. In the April 2006 issue of Arthritis & Rheumatism
noted rheumatology specialists with Kings College London, Dr. Toby Garrood and Dr. Costantino Pitzalis offer an overview of recent breakthroughs and a preview of future directions in this critical quest for specificity.

Among important and promising research, the authors discuss:

Liposome technology, the creation of microscopic vesicles for improved tissue delivery of therapeutic compounds. Liposomes have been successfully used in the imaging of inflamed joints, as well as in dispensing drugs to RA patients. In one animal model experiment, liposome-encapsulated prednisolone was reported to achieve the effects equivalent to 10-fold higher doses of the free drug.

Specific targeting of liposomes to inflamed cells in the synovium. In a novel experiment with a rat model, corticosteroids were encapsulated in RGD peptide liposomes targeted to bind to inflamed cells in the walls of blood vessels. The steroid treatment was delivered rapidly and worked effectively to reduce synovial inflammation, with no signs of the conventional side effects.

Further potential targets within the inflamed joint, including synovial macrophages, cells that work to remove harmful bacteria, and E-selectin, an adhesion molecule in the blood vessel walls that recruits immune-boosting lymphocytes.
Looking forward, Dr. Garrood and Dr. Pitzalis highlight substantial, indirect evidence of the existence of a truly specific synovial homing receptor "the key to unlocking the mechanisms of inflammation" and exciting advances in phage display technology. "Significant progress is being made in the development of technologies for specific targeting of the synovium and delivery of therapeutic agents," the authors attest. They conclude by emphasizing the importance of identifying novel molecular targets within the synovium for optimizing the diagnosis and management of RA.

Editorial: "Targeting the Inflamed Synovium: The Quest for Specificity," Toby Garrood and Costantino Pitzalis, Arthritis & Rheumatism, April 2006, 54:4, pp. 1055-1060.


Questions to explore further this topic:

Where are the joints in a body?

What are joints?

Bones, muscles and joints

How are joints classified?

What are the different types of joints?

Biomechanics of Joints

How are joints lubricated?

What are the joints of the hand?

What is a cartilage?

What is collagen?

What are ligaments?

Ligaments of the hand

Ligaments of the elbow

Ligaments of the knee

What are tendons?

What is the difference between a tendon and a ligament?

What is a synovial joint?


What is a rheumatologist?

How can you take care of your joints?

What is joint stability?

What are the diseases of the joint?

What is arthritis?

What is the difference between arthritis and rheumatism?

What are the different types of arthritis?

What is rheumatoid arthritis?

What is pseudogout?

What is polymyalagia rheumatica?

What is spondyloarthritis?

What is psoriatic arthritis?

What is tendonitis?

What is back pain?

How can one live well with rheumatoid arthritis?

Exercise and arthritis

Diet and arthritis

Are there herbal and natural remedies for arthritis?

Can children have arthritis?

Medications for arthritis














Last edited by adedios on Sat Jan 27, 2007 4:42 pm; edited 4 times in total
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PostPosted: Mon Jul 10, 2006 11:06 am    Post subject: Why Knuckles Crack and Joints Creak Reply with quote

Why Knuckles Crack and Joints Creak

By Corey Binns
Special to LiveScience
posted: 10 July 2006
12:19 am ET

Some peoples' bodies play a percussive symphony of cracking and creaking, thanks to the large orchestra of noise-making human joints. But what's behind it all?

Read the entire article (plus quizzes at the end) at:
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PostPosted: Thu Jul 27, 2006 6:37 am    Post subject: what people with arthritis believe about exercise Reply with quote

John Wiley & Sons, Inc.
27 July 2006

Understanding what people with arthritis believe about exercise

Study of perceived exercise barriers, enablers and benefits suggests ways to increase the rates of regular exercise among arthritis patients
Arthritis is the leading cause of disability in the United States. In total, the treatment and toll of this progressive disease costs our country about $86 billion per year, a figure expected to rise as Baby Boomers age. Among the many approaches to disease management, exercise has been shown to reduce pain, delay disability, and improve physical function, muscle strength, and quality of life. Yet, despite such compelling, well-documented benefits, rates of participation in regular exercise are lower among individuals with arthritis than those without it.

Understanding what motivates and enables some people with arthritis to exercise, and what prevents others, is the focus of a study featured in the August 2006 issue of Arthritis Care & Research ( Conducted at the University of South Carolina, and supported by a grant from the Centers for Disease Control and Prevention and the Association of Schools of Public Health, its findings have direct implications for how to market exercise to arthritis patients, how to tailor exercise programs to their challenges, and how to encourage and sustain their participation.

To identify the perceived barriers to and benefits of exercise among people with arthritis, 68 people with arthritis were divided into 12 focus groups. To help participants feel more comfortable and willing to talk openly, the groups were segmented by exercise status, socioeconomic status, and race. Each focus group came together and discussed their perceptions of exercise, as well as their experiences. Each discussion was transcribed and coded by two people. Following the sessions, NVivo software was used to extract themes for exercisers with arthritis, defined by participation in moderate activities on at least 3 days per week for 30 minutes per day or vigorous activities on at least 3 days per week for 20 minutes per day or strength training on at least 3 days per week for 20 minutes per day, and for non-exercisers with arthritis. Among them:

Pain. Although all focus groups stressed pain as a barrier, exercisers were more likely to make adaptations and work through the pain to attain the benefits of exercise, while non-exercisers were more likely to give up exercise altogether.

Attitudes and beliefs. Non-exercisers were much more likely than exercisers to express the belief that they were physically unable to exercise.

Lack of support. Non-exercisers were more likely to cite their physician's failure to refer them to helpful exercise programs and to voice their desire for exercise partners with similar limitations.

Lack of programs. For both exercisers and non-exercisers, the lack of exercise programs or facilities for individuals with arthritis emerged as a barrier.

Symptom management. Exercisers tended to be more positive about how exercise could reduce pain, improve mobility, and more, because they had experienced these benefits. Non-exercisers often used such phrases as "this is what I hear" or "this is what I understand" to describe desired outcomes.

"Our findings provide useful information for understanding the experiences with and beliefs about exercise among persons with arthritis," notes study author, Sara Wilcox, Ph.D., "and informing recruitment and intervention strategies." To increase the rates of regular exercise among arthritis patients, Dr. Wilcox and her colleagues offer concrete recommendations for health care professionals and communities, including:

Make a practice of prescribing exercise, with referrals and instruction.
Work to expand the availability of arthritis-specific exercise programs.
Emphasize ways in which individuals with arthritis can modify exercise to accommodate their physical limitations and effectively manage the pain.
Move beyond knowledge-based approaches to change the mindsets and behavior of non-exercisers.

Article: "Perceived Exercise Barriers, Enablers, and Benefits Among Exercising and Nonexercising Adults With Arthritis: Results From a Qualitative Study," Sara Wilcox, Cheryl Der Ananian, Jill Abbott, JoEllen Vrazel, Cornelia Ramsey, Patricia A. Sharpe, and Teresa Brady, Arthritis Care & Research, August 2006; (DOI: 10.1002/art.22098).
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PostPosted: Mon Oct 30, 2006 8:14 pm    Post subject: Turmeric supplements show promise in treating arthritis Reply with quote

John Wiley & Sons, Inc.
30 October 2006

Turmeric supplements show promise in treating arthritis

More than 40 percent of arthritis sufferers in the U.S. report using complementary and alternative medicine, including dietary supplements, and the use of alternative remedies has increased since the FDA issued health warnings about anti-inflammatory drugs such as Celebrex. However, the effectiveness of many supplement ingredients has not been adequately studied. To complicate the matter, over-the-counter supplements are not regulated in the same way as drugs and their composition can vary widely. A new study published in the November 2006 issue of Arthritis & Rheumatism ( examined the effect and mechanism of turmeric (a botanical supplement long thought to have anti-inflammatory properties) on arthritis.

Led Janet L. Funk and Barbara N. Timmermann (currently at the University of Kansas), researchers at the University of Arizona in Tucson, AZ had already shown in an earlier study that turmeric can prevent joint inflammation in rats. In the current study, they expanded their research to compare the chemical composition of an experimental turmeric extract with those of commercially available over the counter turmeric dietary supplements. They also examined the dosage of the experimental version on joint inflammation and destruction, determined its effect on inflammation markers, and ascertained the mechanism by which turmeric protects joints in arthritis.

Initial results showed that a version of turmeric extract that was free of essential oils had a significant impact on arthritis and most closely matched the composition of commercially available supplements. This version was used in subsequent experiments and was shown to prevent acute and chronic arthritis, even when it was administered after arthritis had been induced. In addition, turmeric significantly inhibited joint destruction due to arthritis, and inhibited NF-B, a protein that controls the gene expression of substances that produce an inflammatory response. Turmeric also altered the expression of hundreds of genes involved in joint swelling and destruction and prevented an increase in osteoclasts (cells that break down bone) in joints.

The current research, which was funded by the Office of Dietary Supplements and National Center for Complementary and Alternative Medicine of the National Institutes of Healthis the first study to document the composition of a turmeric-containing compound that is similar to commercially available products and to document the mechanisms by which it reduces the effects of arthritis. The authors were able to find an effective dose in rats that would be equivalent in humans to 1.5 milligrams per day of a portion of the turmeric root that makes up 3% of dried turmeric powder. The inhibition of NF-B and of key inflammatory genes directly or indirectly activated by NF-B suggests that inhibition of this protein may be an important mechanism in turmeric's anti-arthritic effects. In fact, the authors state that "it would appear that turmeric dietary supplements share the same mechanism of action as antiarthritic pharmaceuticals currently under development that target NF-B." It is also possible that turmeric blocks other inflammatory pathways, given its chemical complexity. Turmeric seems to block early inflammatory responses, as evidenced by the fact that it was effective when started 3 days but not 8 days after arthritis was induced, the authors note.

"In summary," the authors state, "just as the willow bark provided relief for arthritis patients before the advent of aspirin, it would appear that the underground stem (rhizome) of a tropical plant [turmeric] may also hold promise for the treatment of joint inflammation and destruction." They note that the anti-inflammatory effects of botanicals can only be utilized if their chemical content is analyzed. The authors conclude: "Finally, before turmeric supplements can be recommended for medicinal use, clinical trials are clearly needed to verify/determine whether treatment with adequate doses of well-characterized turmeric extracts can indeed prevent/suppress disease flares in RA [rheumatoid arthritis] patients, as well as to explore any potential benefits of turmeric dietary supplements in the prevention or treatment of more common forms of arthritis in the general population."

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PostPosted: Wed Mar 28, 2007 6:48 am    Post subject: Arthritis pain, the brain and the role of emotions Reply with quote

John Wiley & Sons, Inc.
27 March 2007

Arthritis pain, the brain and the role of emotions

Arthritis pain is processed in brain areas concerned with emotions and fear, finds study, indicating target for pain-relieving therapies
How does the brain process the experience of pain? Thanks to advances in neuroimaging, we now know the answer lies in a network of brain structures called the pain matrix. This matrix contains two parallel systems. The medial pain system processes the emotional aspects of pain, including fear and stress, while the lateral system processes the physical sensations—pain's intensity, location, and duration.

Marked by morning stiffness, joint aches, and flare-ups, the pain of arthritis tends to be acute and recurrent, in contrast to many chronic pain conditions. Arthritis pain therefore makes an ideal model for comparing common clinical pain with experimental pain. Inspired by this observation, researchers at University of Manchester Rheumatic Diseases Centre in the United Kingdom conducted the first study to compare directly the brain areas involved in processing arthritis pain and experimental pain in a group of patients with osteoarthritis (OA). Their results, published in the April 2007 issue of Arthritis & Rheumatism (, shed light on the role of emotions in how patients feel arthritis pain.

The study focused on 12 patients with knee OA—6 women and 6 men, with a mean age of 52 years. All subjects underwent positron emission tomography (PET), to measure and map 18F-fluorodeoxyglucose (FDG) uptake in the brain as an indicator of brain activity. PET scans were performed during three different pain conditions: arthritic knee pain; experimental pain, achieved by heat application; and pain-free. The brain responses to each pain state were then rigorously examined and statistically evaluated and compared for significant differences.

In all OA subjects, both pain conditions activated the entire pain matrix. However, during arthritic pain, activity was increased within the medial pain system of the brain, including most of the cingulate cortex, the thalamus, and the amygdala. This suggests that, for these patients, arthritis pain has more emotional impact—and perhaps stronger associations with fear and distress—than experimental pain. Arthritis pain also prompted heightened activation of the prefrontal cortex and the inferior posterior parietal cortex, areas of the brain instrumental in the supervision of attention. Their activation while suffering arthritis pain may reflect the patients' concentration on coping strategies.

"The present study demonstrates the importance of the medial pain system during the experience of arthritic pain and suggests that it is a likely target for both pharmacologic and nonpharmacologic interventions," notes its leading author, Prof. A.K.P. Jones. "Considering the recent concerns about the long-term safety of cyclo-oxygenase inhibitors, we hope that our current findings will stimulate partnerships between academia and the pharmacological industry to develop a new class of analgesics for arthritic pain that specifically target the medial pain system."

As Prof. Jones acknowledges, the study's main limitation is its small number of subjects. Larger studies of the relationship between arthritis pain and the medial pain system are critical, particularly for exploring the effect of variables from depression and anxiety to guided imagery, meditation, and other mind-based pain management techniques. "Researchers should be moving toward more naturalistic studies in patients," Prof. Jones suggests, "in order to fully understand the perception of different types of clinical pain."

Article: "Arthritic Pain Is Processed in Brain Areas Concern With Emotions and Fear," B. Kulkarni, D.E. Bentley, R. Elliott, P.J. Julyan, E. Boger, A. Watson, Y. Boyle, W. El-Deredy, and A.K.P. Jones, Arthritis & Rheumatism, April 2007; (DOI: 10.1002/art.22460).
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PostPosted: Sun Apr 29, 2007 9:53 am    Post subject: Green tea compound may be a therapy for people with rheumato Reply with quote

University of Michigan Health System
29 April 2007

Green tea compound may be a therapy for people with rheumatoid arthritis

Anti-inflammatory compound inhibits production of molecules that cause destruction of cartilage, bone
ANN ARBOR, Mich. -- A new study from the University of Michigan Health System suggests that a compound in green tea may provide therapeutic benefits to people with rheumatoid arthritis.

The study, presented April 29 at the Experimental Biology 2007 in Washington, D.C., looks at a potent anti-inflammatory compound derived from green tea. Researchers found that the compound -- called epigallocatechin-3-gallate (EGCG) -- inhibited the production of several molecules in the immune system that contribute to inflammation and joint damage in people with rheumatoid arthritis.

The compound from green tea also was found to suppress the inflammatory products in the connective tissue of people with rheumatoid arthritis.

"Our research is a very promising step in the search for therapies for the joint destruction experienced by people who have rheumatoid arthritis," says Salah-uddin Ahmed, Ph.D., lead researcher on the study. Ahmed, a research investigator with the Division of Rheumatology at the U-M Health System, was selected to present the research at the Experimental Biology meeting as the recipient of the Young Scientist Travel Award, given by the American Society for Pharmacology and Experimental Therapeutics. This study was also selected by the American Society for Nutrition to be featured in a press release.

To conduct the research, the scientists isolated cells called synovial fibroblasts from the joints of patients with rheumatoid arthritis. These fibroblasts -- cells that form a lining of the tissue surrounding the capsule of the joints -- then were cultured in a growth medium and incubated with the green tea compound.

The fibroblasts were then stimulated with pro-inflammatory cytokine IL-1ƒÒ, a protein of the immune system known to play an important role in causing joint destruction in people with rheumatoid arthritis.

The researchers looked at whether the green tea compound has the capability to block the activity of two potent molecules, IL-6 and cyclooxygenase-2 (COX-2), which also are actively involved in causing bone erosion in the joints of people with rheumatoid arthritis.

When untreated cells were stimulated with IL-1ƒÒ, a sequence of molecular events occurred that resulted in production of the bone-destructive molecules. But the scientists found that pre-incubation with EGCG was capable of inhibiting the production of these molecules. EGCG also inhibited the production of prostaglandin E2, a hormone-like substance that causes inflammation in the joints.

The cell signaling pathways that regulate levels of these immune system molecules under both normal and rheumatoid arthritis situations are well studied, and the researchers were able to trace the effects of the green tea compound infusion to see that it worked by inhibiting these pathways.

Ahmed says that these studies suggest that EGCG or molecules that could be derived synthetically from the EGCG found in green tea may be of therapeutic value by inhibiting the joint destruction in rheumatoid arthritis.

Previously, Ahmed and other researchers made another promising finding when EGCG-pretreated synovial fibroblasts were stimulated with the cytokine IL-1ƒÒ to study the protective effect of this green tea compound. Compared to untreated synovial fibroblasts, the cells treated with EGCG markedly blocked the ability of IL-1ƒÒ to produce the proteins and enzymes that infiltrate the joints of persons with rheumatoid arthritis and cause cartilage degradation.

The laboratory now is focused on the inhibitory role of EGCG in gene expression. The scientists plan to test EGCG in animal models of rheumatoid arthritis to see if it provides similar therapeutic or preventive effects. Ahmed believes that the outcome of these studies will form a strong foundation for future testing of green tea compound in humans with rheumatoid arthritis.

In addition to Ahmed, authors of the study are Angela Pakozdi, M.D., a former research fellow in the Division of Rheumatology at the U-M Health System; and Alisa E. Koch, M.D., the Frederick G.L. Huetwell and William D. Robinson, M.D. Professor of Rheumatology at the U-M Health System and a researcher at the Veterans Affairs Ann Arbor Healthcare System.

This research was supported by National Institutes of Health grants and Veteran Administration Medical Research Service funds to Koch.

Meeting: Experimental Biology 2007, American Society for Nutrition Abstract 1652.
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PostPosted: Thu Jun 14, 2007 9:27 am    Post subject: Aggressive nature of hand osteoarthritis Reply with quote

European League Against Rheumatism

Aggressive nature of hand osteoarthritis

Highlighted by new study

Barcelona, Spain, Thursday 14 June 2007: In just two years, patients with hand osteoarthritis (OA) experienced a significant increase in pain and functional limitations, according to new data presented today at EULAR 2007, the Annual European Congress of Rheumatology in Barcelona, Spain. Statistically significant radiological progression was also detected in 20% of subjects.

OA is the most common form of arthritis. It generally affects older people, especially women and can occur in multiple areas of the hand and wrist, causing pain and stiffness and affecting everyday activities requiring fine motor control and hand grip e.g. writing. Over time, if left untreated, the bones that make up the joint can lose their normal shape, causing further pain and limited motion. However, knowledge about the progression of hand OA and effective therapies to prevent its progression has been lacking.

Led by Dr Stella Botha-Scheepers of Leiden University, The Netherlands, this study followed 172 patients (mean age 60.5 years, 78.5% women) with hand OA (defined by the American College of Rheumatology criteria) for two years, assessing: pain intensity upon lateral pressure in the DIP, IP, PIP and CMC 1 joints on a four-point scale; self-reported hand pain and functional limitations with subscales of the Australian/Canadian Osteoarthritis Hand Index (AUSCAN LK 3.0); and osteophytes and joint space narrowing in the right and left DIP joints, IP joints of the thumbs, PIP joints and CMC 1 joints through standardized radiographs.

Despite a relatively short follow-up period of two years, statistically significant increases in pain intensity on lateral pressure standard response mean (SRM) 0.67), AUSCAN pain scores (SRM 0.25) and AUSCAN function scores (SRM 0.23) occurred. Statistically significant radiological progression was also seen in 20% of patients, in terms of joint space narrowing (SRM 0.34) and osteophytes (SRM 0.35), with progression of osteophytes occurring more often in women and middle-aged patients, and especially in women in an early post-menopausal stage.

Dr Botha-Scheepers commented: “The findings of this study underline the critical need for early, effective intervention in hand OA to prevent irreversible progression, given the dramatic deterioration of clinical and radiological disease status seen in just two years.”

Hand OA tends to appear in a predictable pattern, most commonly affecting the small joints of the fingers and the joint at the base of the thumb. It can be diagnosed by medical examination and X-rays of the hand. Treatment options for arthritis of the hand and wrist include oral medication, injections, splinting and surgery.

For further information on this study, or to request an interview with the study lead, please do not hesitate to contact the EULAR congress press office on:
Rory Berrie: Onsite tel: +44 (0) 7900 698 946
Camilla Dormer: Onsite tel: +44 (0) 7725 328 983

Abstract number: OPO029


The European League Against Rheumatism (EULAR) is the organization which represents the patient, health professional and scientific societies of rheumatology of all the European nations.

The aims of EULAR are to reduce the burden of rheumatic diseases on the individual and society and to improve the treatment, prevention and rehabilitation of musculoskeletal diseases. To this end, EULAR fosters excellence in education and research in the field of rheumatology. It promotes the translation of research advances into daily care and fights for the recognition of the needs of people with musculoskeletal diseases by the governing bodies in Europe.

Diseases of bones and joints, such as rheumatoid arthritis and osteoarthritis cause disability in 4 - 5 % of the adult population and are predicted to rise as people live longer.

As new treatments emerge and cellular mechanisms are discovered, the 8th Annual European Congress of Rheumatology in Barcelona (EULAR 2007) brings together more than 10,000 experts - scientists, clinicians, healthcare workers, pharmaceutical companies and patients - to share their knowledge in a global endeavour to challenge the pain and disability caused by musculo-skeletal disorders.

To find out more information about the activities of EULAR, visit:
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PostPosted: Tue Nov 06, 2007 6:20 pm    Post subject: First-Ever Study: Lack of Critical Lubricant Causes Wear in Reply with quote

First-Ever Study: Lack of Critical Lubricant Causes Wear in Joints
6 November 2007
Brown University

For the first time, researchers have linked increased friction with early wear in the joints of animals. Work led by Brown University physician and engineer Gregory Jay, M.D., shows mice that do not produce the protein lubricin begin to show wear in their joints less than two weeks after birth. This finding not only points up the protective power of lubricin but also suggests that it could be used to prevent joint wear after an injury.

PROVIDENCE, R.I. [Brown University] — 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.
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