Effects of exercises, inflammatory markers, rising treatments—we’ve got the latest on cartilage health in this article.
In this article:
- Exercise Is Bad for Your Bones, They Say…
- The Cartilage Connection
- Inflammatory Pathways
- PGE2 Receptors Revisited
- Promising Cartilage Repair Treatments
- A Silver Lining for Osteoarthritis and Other Joint Cartilage Condition
The Science of Cartilage Health
Exercise Is Bad for Your Bones, They Say…
Should we exercise? Some may say “no.”
Here’s their theory: the body— bones, muscles, organs—is built to withstand a predetermined number of hours of wear and tear. Once this limit is reached, part by part, the body fails.
By speeding up the timetable with the stresses of exercise, we contribute to a shorter lifespan.
True, there are variations in human lifespans but, according to this theory, they are attributable to the effects of good genes, “super genes,” creating body parts that can withstand more abuse. These theorists put more emphasis on diet and essential multivitamins, rather than exercise or a combination thereof.
“Do we contribute to a shorter lifespan with the stresses of exercise?”
Although it may be appealing to think that it’s “healthier” not to expend energy and work up a sweat a few times a week, there is quite a bit of evidence to the contrary. Here’s just one example.
Exercise, especially aerobic exercise, has been shown to have a significant positive effect on cardiovascular health: improving vascular tone and lipid profile (raises HDL), as well as reducing the work (beats per minute) the heart has to perform (a strong-healthy heart has a lower resting heart rate).
Aside from the fact that it’s an excellent means of healthy weight control, recent research has also demonstrated that moderate exercise, such as running and walking, can actually improve the health of cartilage tissue. Can this help reduce/prevent the aches and pains associated with aging joints?
The Cartilage Connection
Adequate cartilage tissue at the ends of our bones allows for smooth, low friction, pain-free movement of our limbs. Moderate exercise seems to stimulate cartilage growth, improving the cushion of cartilage at the points of articulation. (Exercise also improves muscle tone and strength to keep our joints aligned, preventing damage.)
“Chronic joint stress may lead to the development of osteoarthritis (OA).”
However, exercise that produces repetitive pounding of the joint surfaces, especially with excess weight, seems to have the opposite result: cartilage damage. This kind of chronic stress may lead to the development of one of the most common diseases of modern western civilization, osteoarthritis (OA).
Although the incidence of this disease appears to be increasing (perhaps due, in part, to an increasingly obese population), our knowledge of it was limited…until recently.
Numerous investigators have reported markers of inflammation (IL-6, IL-1, TNF alpha) in the cartilage tissues of patients with OA. However, the biochemical mechanism(s) involved in the destruction of cartilage during the disease’s initiation and progression has not been clear.
A recent study revealed not only a number of intricate biochemical events leading to the destruction of cartilage, but also the probable cause of the pain associated with OA. The study, using a model system of OA, placed human chondrocytes (cartilage cells) in a specialized chamber to mimic the high shear stress conditions that lead to OA.
“Cytokine IL-6 is believed to be responsible for the pain associated with OA.”
In response to the stress, a fatty acid-like inflammatory substance, (PGE2) was produced, as well as specific receptors to which it binds. This PGE2-receptor binding event triggered a series of specific chemicals and enzymes, which activated the master regulator of inflammation, NF-kB.
The NF-kB (a transcriptional factor controlling gene expression) travels to the nucleus of the cartilage cell and turns on genes, carrying the code for several inflammatory agents, including cytokine IL-6.
The cytokine IL-6 is believed to be responsible for the pain associated with OA. And the series of reactions, initiated by stress on cartilage, appear to produce destructive machines, proteases, capable of tearing apart the constituents of cartilage.
PGE2 Receptors Revisited
Previous work also showed that large amounts of PGE2 were present in cartilage from patients with OA, identifying it as the principal substance that led to the disease.
In fact, this hypothesis was popular about 30 years ago, when some orthopedists were prescribing aspirin for OA patients. They believed this inhibitor of the enzyme responsible for PGE2 production (cyclo-oxygenase or COX-2) would not only relieve the pain, but also help cure the disease.
The more recent study demonstrates, however, that stress on cartilage not only increases the levels of PGE2, but also affects the levels of two important receptors for it, namely EP2 and EP3. The former, EP2 (increases with stress), activates the pathway leading to cartilage destruction.
The latter, EP3 (decreases with stress), inhibits this pathway.
In other words, the destructive process is not the result of more PGE2 alone, but also more EP2, and less EP3.
Cartilage destruction is prominent in osteoarthritis (OA). OA is commonly associated with obesity, misaligned joints, excessive trauma to joints (sports injury), and too much repetitive activity. All of these cause significant stress to the cartilage, the chondrocytes, which respond by attempting to “remodel” the cartilage to make it stronger.
Unfortunately, cartilage synthesis seems to be inhibited.
“The answer brings us back to the value of moderate exercise.”
How can we avoid the stress that starts the destructive chain reaction and promote cartilage growth? The answer for both brings us back to the value of moderate exercise, like walking (also running as long as it is of moderate intensity and your joints are healthy).
It’s a great form of healthy weight control and is probably the most important method of prevention. It strengthens the muscles, ligaments, and tendons that help keep the joints properly aligned.
And it stimulates cartilage growth.
Are there other ways to improve cartilage health?
Reported clinical studies have shown limited improvement in some OA patients taking the supplement chondroitin sulfate/glucosamine. Other natural sources currently being examined as potential OA therapeutics include plant-derived compounds such as curcumin (turmeric flavonol), a number of polyphenols like pycnogenol and resveratrol, and the omega-3 fatty acids EPA/DHA.
Polyphenols Definition: These are plant compounds with antioxidant properties offering various health benefits
Thanks to research like the study described earlier, a better understanding of the events leading to cartilage destruction and OA may lead to the development of new cartilage defect treatments for this painful and debilitating disease.
Promising Cartilage Repair Treatments
Part of the continuous advancement of research on OA and other cartilage conditions is the surfacing of promising cartilage repair treatments. These therapies aim to harness the body’s healing abilities to repair damaged cartilage.
Although expensive, they may help relieve symptoms or slow down the progression of cartilage damage in OA patients.
1. Osteochondral Autograft or Allograft Transfer System or OATS
This treatment repairs the hyaline cartilage, the affected area of the synovial joint in OA, by:
- Autograft – transferring a plug of bone and cartilage from a healthy part of the knee to the damaged area; or
- Allograft – using donated tissues on the damaged area
In one study, researchers found the OATS technique to be an appropriate hyaline cartilage defect treatment to avoid symptom progression.
The OATS technique is recommended for active people ages 15-50 with small and distinct cartilage damage.
This an older technique in which surgeons clean and smoothen the tear edges of the joint cartilage and pierce holes in the underlying bone. This will form blood clots rich in stem cells and growth factors.
Overtime the clots will form into fibrocartilage, a less supple and durable cartilage.
The microfracture technique is ideal for patients below 40 and with cartilage defects smaller than 4 cm.
3. Autologous Chondrocyte Implantation (ACI)
This is a two-part surgical procedure for the hyaline cartilage.
First, an orthopedic surgeon arthroscopically removes a tiny piece of healthy cartilage from the patient’s knee joint. It is then cultured to produce millions of new cartilage cells.
Six to eight weeks after, open surgery is performed to fit and seal a collagen patch over the defective cartilage and inject the cultured cells.
ACI may help patients with early osteoarthritis reduce pain and improve function. In one study following 155 OA patients, researchers found that 92% of the subjects were functioning well five years after the procedure and the need for a joint replacement was delayed.
4. Stem Cell Therapy and Other Experimental Trends
Part of the existing trends in treating cartilage defects is the use of stem cell technology and other biomedical procedures such as the following:
Mesenchymal Stem Cell Injection
Mesenchymal stem cells (MSCs) found in the bone marrow can be grown into cartilage cells. There are existing procedures wherein a patient’s bone marrow concentrate is injected into the damaged areas aiming to repair the defect.
While there are significant results on both animal and human subjects, stem cell treatments for OA are still experimental. More randomized trials are needed to establish their therapeutic effects for arthritis.
Platelet-Rich Plasma Therapy
Another OA treatment rising into popularity is platelet-rich plasma (PRP) therapy. In this minimally invasive treatment, a doctor draws the patient’s blood, separates and concentrates the platelets, and injects the solution into the affected area.
The PRP solution contains growth-factors that may help reduce inflammation and promote tissue repair. Much like stem cell therapy, there are positive results reported in some studies but further research is still needed to establish the procedure’s effectiveness.
A Silver Lining for Osteoarthritis and Other Joint Cartilage Conditions
Osteoarthritis (OA) affects cartilage, the resilient material that covers the ends of bones and is necessary for near-frictionless flexion and extension. The end result of the disease is a joint surface eroded to the underlying bone.
The affected joint has a high coefficient of friction, making movement without excruciating pain difficult. OA is commonly associated with excessive stress placed on the cartilage, either by blunt trauma (sports injury), or excessive stress due to repetitive pounding (such as excessive running), or obesity.
With the goal of providing information that could lead to new therapeutics for OA, a group of investigators set out to determine how one of the inflammatory agents associated with the disease, the cytokine IL-6, is activated during its early stages. The team, from Johns Hopkins University and the George Washington University Medical Center, published “Shear-induced interleukin-6 synthesis in chondrocytes: the roles of E prostanoid (EP)2 and EP3 in cAMP/protein kinase A- and PI3-K/Akt-dependent NF-kB activation,” in the Journal of Biological Chemistry.
The article describes the investigators’ discovery of a complicated biochemical pathway. With an OA model system, designed to mimic the effects of stress on the cartilage that would normally initiate the disease in humans, the researchers examined the expression of several genes in cartilage cells, chondrocytes, compared to chondrocytes under non-stress conditions.
The results showed a remarkable increase in several substances previously demonstrated to be up-regulated in OA cartilage. More importantly, the experiments revealed a sequence of events in the stressed chondrocyte, starting with an increased synthesis of the enzyme COX2 (cyclo-oxygenase 2), which in turn is responsible for the production of the inflammatory fatty acid substance, PGE2.
Coincident with the synthesis of PGE2 was increased synthesis of its receptor, EP2. The binding of PGE2 to EP2 initiated production of the signaling molecule cAMP, which in turn, activated a cascade of enzymes, culminating in the activation of the master regulator of inflammation, NF-kB.
NF-kB, transported to the nucleus of the cell, activated specific inflammatory genes, including IL-6, as well as additional inflammatory cytokines. These activated specific cartilage proteases, producing destruction of cartilage and the characteristic OA condition (joint pain and decreased mobility).
The researchers speculate that their data on this biochemical pathway may lead to therapeutics for early intervention in cartilage erosion, allowing OA to be more easily controlled.
This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.
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Dr.Treadwell answers your questions.
Question: I am a long-time customer and am extremely pleased with the Juvenon products. In a discussion with a friend the other day, he said he was contemplating taking human growth hormone. Can you give me any info about the use of human growth hormone? – D
Answer: Although the claims for human growth hormone (HGH) may seem enticing, I don’t recommend taking it, except for a specific disorder and under a qualified health professional’s supervision. Why? It’s expensive and, apart from some human studies that showed increased lean body mass, most of the evidence for the benefits of HGH is anecdotal. On the other hand, negative side effects, including cancer cell growth, have been documented in animal studies. In my opinion, it’s not worth the gamble.
Benjamin V. Treadwell, Ph.D.,is a former Harvard Medical School associate professor and member of Juvenon’s Scientific Advisory Board.
Editor’s Note: This post article was originally published on June 10, 2010, and has been updated for quality and relevancy.