We’ve blogged many times in the past about how biomechanics are generally ignored by our medical system and how the mechanics of the body impacts things like arthritis. This issue of how subtle abnormalities of body movement can cause arthritis is discussed in more detail in our medical practice’s book, Orthopedics 2.0. A study out last month again confirms that small differences in how the body moves can add up and cause very big problems. The study looked at more than 3,000 patients aged 50-79 years and found that when the length of their legs was off by more than 1 cm (about 1/3 of an inch), the risk of having knee arthritis in the shorter leg was about doubled when compared to patients with legs that were equal length, causing “short leg knee arthritis”. Why? The shorter leg takes slightly more impact on walking, so it makes sense that over years, millions of these tiny increases in impact can wear away more cartilage on that side. The solution? First, have your leg lengths measured by your doctor. If they’re off by more than 1 cm, than consider getting a heel lift on the shorter leg to make your legs more of an equal length. Also realize that for some patients who’ve had a difference in leg lengths for a long time, other parts of the body may have adapted to the unequal leg length. In these patients, we’ve noticed that correcting the leg length may cause a flare-up of pain in the back or neck. This is because the spine (note the picture above that shows how a leg length discrepancy puts a side bend in the spine) curves to adapt to the short leg. The upshot? Check your leg length and if you know you have a difference, get it corrected before years of being “off kilter” cause the rest of your body to adapt to the shorter leg!
I’m always asked by our stem cell patients, what supplements do we recommend to prevent cartilage loss or build cartilage? Well a new, well designed study out this week may have answered that question. This study had patients take either Condoitin Sulfate or a placebo and then tracked cartilage volume measured with a special MRI. Chondroitin is a “GAG” (glycosaminoglycan) which is an important structural component of cartilage, so it’s been recommended to arthritis patients for years. While many patients and physicians swear by it, the medical research studies on Chondroitin have been all over the map, with some showing good efficacy for arthritis patients and others not showing any differences from placebo. Of note, the National Institutes of Health conducted a study and found no effects for Chondroitin for lessening arthritis symptoms when compared to a sugar pill. However, the study design was a bit “Pharma-centric”. For example, the NIH study compared Glucosamine and Chondroitin (GCS) to the blockbuster drug Celebrex. The problem with this study design is that pitting a nutritional supplement against Celebrex is like comparing a ball peen hammer to a sledgehammer for nailing abilities. Both will work, with the ball peen hammer (GCS) taking a bit longer to seat the nail and the Sledgehammer (Celebrex) working more dramatically, but with significant collateral damage. This is exactly what the NIH observed; Celebrex produced big gun effects for lowering pain in all arthritis categories, while Glucosamine plus Chondoitin worked only for patients with moderate to severe pain. Since GCS had no effect on all arthritis patients (the mild, moderate, and severe groups), the study authors concluded that GCS didn’t work. While Celebrex worked well in all groups, other studies have shown convincingly that it also increases your sudden death and heart attack risks to a dangerous level.
While it would seem the NIH study was conclusive, it failed to answer an important question. For those patients with mild pain who take supplements for prevention, does Chondroitin do anything? The answer seems to be “yes” based on the new MRI research. The researchers in the new study took 69 arthritis patients and randomized them at multiple centers to receive either a placebo pill or Condroitin Sulfate 800 mg once a day for 6 months. They then took the additional step of giving both groups Chondoitin for an additional 6 months. MRI cartilage volume was measured before and after (to see if the supplement had any impact on preserving cartilage). The Chondroitin group showed significantly less cartilage volume loss at 6 months on MRI when compared to the placebo. This difference in MRI detected cartilage loss persisted at the 12 month mark as well. The Chondroitin group also had less swelling in the bone marrow (an indication that the cartilage was functioning better due to the Chondroitin). The full text of the article is available here. This study may fit well with the study I blogged on earlier showing that a reduction in the SIRT-1 gene activation reduced GAG production, making cartilage unstable. Both of these studies taken together may provide insights into how cartilage turnover works and interacts with diet. For example, you can either put more building blocks in the hopper (take cartilage components like Chondoitin) or stimulate the genes that make new GAG’s (like Chondroitin and Glucosamine) by taking Resveratrol. Either way, the cartilage health and durability is improved. The upshot? Since MRI studies are objective with endpoints that are easy to measure and pain studies are subjective with end points that are hard to measure, I would say this new study blows the socks off the old NIH study in that it’s more in line with why patients take supplements-to keep from getting arthritis or to reduce it’s worsening. So until another study comes out (this one could be bigger), I would say take your 800 mg Chondroitin everyday!
We don’t much care where you get your stem cells, as long as the source of the stem cells matches the tissue you’re trying to repair. The problem with stem cells is that certain sources produce stem cells more capable of repairing certain tissues and stem cells from other sources are less capable. The general rule of thumb is, the closer the stem cells are to the structure in need or repair, the better they are at repairing that area. This makes sense at face value, as these resident stem cells in all of our tissues have a role in maintaining and repairing that local organ or tissue. As an example, fat stem cells from your belly or thigh would be good at repairing the local tissues like skin, nerves, blood vessels, etc… So it wasn’t surprising to see yet another study showing that bone marrow stem cells are better at repairing bone than fat based stem cells. This fits with many other studies showing that bone marrow stem cells are much better at repairing orthopedic tissues than fat derived stem cells. This again makes sense, as why would stem cells from belly fat have any role in repairing bone? At the end of the day, rooting for one type of stem cell because that’s all the doctor knows how to harvest is like rooting for only one stem cell sports team and not recognizing that all stem cell teams have their positives and negatives. For example, stem cells derived from fat are much better for cosmetic work and structural fat grafts than stem cells derived from bone marrow. So why fit a square peg into a round hole or use a hammer when a wrench is needed? Use the stem cell source that fits the job!
Yet another study on the link between removing parts of the knee meniscus in menisectomy (athropscopy) knee surgery. These researchers looked at few different studes and summarized their results. They concluded that, “The amount of removed meniscus is the most important predictor factor for the development of osteoarthritis.” In other words, taking out more meniscus during knee surgery is correlated with more arthritis of the knee going forward. This conclusion fits with the opinions of other researchers that have shown the same connection between knee meniscus surgery and arthritis of the knee. How should this influence patient decision making? If knee surgery is planned and you’re tied to the concept that this is the only thing that will help your knee, ask the surgeon if he plans to remove torn parts of the meniscus. Ask these questions even if you’re told that the surgeon plans a “meniscus repair”, as many surgeons won’t try to repair the tears in the “white zone” of the meniscus without blood supply (this is 2/3′rds of the meniscus). In addition, request that the surgeon not remove any pieces of the meniscus or to try to remove as little as possible. As always, we would question the efficacy of the concept of knee surgery for meniscus tears in all but the most extreme circumstances. Our opinion would be to try newer biologic alternative injections like PRP, stem cells, etc… rather than knee surgery for a torn meniscus.
Fascinating, but not surprising study, weighing in on the belief by many physicians (and patients) that x-ray or MRI findings are good at explaining why a patient has pain-in this case focused on shoulder x-ray findings. It might surprise most people to learn that the width of the cartilage remaining in their shoulder joint or the amount of bone spurs doesn’t correlate to pain or function, meaning patients with little joint width left or many bone spurs were no more likely to have pain or lost function than those without those findings. This fits with many other studies in the knee and low back that show the same thing: findings on imaging studies such as MRI and x-ray often don’t tell us why the patient hurts. In the knee for example, 60% of middle aged or elderly patients with meniscus tears had pain and 60% of patients with meniscus tears had no pain. This whole concept needs to start changing our approach to orthopedic care as I have discussed in our practice’s book on regenerative medicine and stem cells-Orthopedics 2.0. We as physicians need to stop believing that a picture is a substitute for a good history and comprehensive physical exam. As doctors, our thumbs are often better (a hands on exam) at determining where the pain might be coming from than an MRI.
What was interesting about the study was that one bone spur did correlate with lost function. This is the bone spur at the bottom of the shoulder joint often seen in patients with advanced shoulder arthritis. This makes sense, as this bone spur would retrict lifting the arm up and above the head, as it would get in the way of the ball moving downward in the socket as the arm moves upward. We’re beginning to work on non-surgical solutions for removing this bone spur using barbotage, to see if getting rid of this spur through a needle may help these patients have better shoulder ranage of motion without the need for surgery.
You know the saying, “there is no free lunch”? Well, several recent studies have rained on the parade of the embryonic stem cells and IPS crowd. A recent piece in the LA times quoting a paper published this week was more percipitation. The problem is that these cell lines have inherent genetic problems. This means that the cells don’t have normal genes, which raises the specter of unintended consequences when these cells are used for therapy (the biggest being cancer). The reason should be clear by now. Embryonic stem cells (or likely even adult stem cells) that are “immortalized” (artificially tricked into growing forever so that they can be mass produced like an antibiotic) pick up these genetic abnormalities because these cells were never designed by nature to have the DNA repair mechanisms that would allow them to be grown for these great lengths of time. For example, everyday, dividing cells in your body pick up back pieces of DNA or errors. We have enzymes that help repair the damage and a secondary line of defense (called the immune system) to yank the malfunctioning cells out of circulation. However, embryonic (or even adult stem cells) were never designed with the mechanisms to be grown for thousands of generations. An embryo is conceived, it grows bigger, and eventually a baby with adult stem cells is born. Nowhere in there was the embryo designed to grow embryonic stem cells for years for the purposes of satisfying a human need for mass produced biologic tissue. How about IPS cells? For those of you who are unaware, IPS means induced pluripotency, which is a fancy way of saying that a normal adult cell is turned into a cell that resembles an embryonic stem cell. Now since this doesn’t even happen in nature, the process of tricking a cell to revert back to the properties of a stem cell is bound to have issues (which many IPS researchers have been very honest about from the start). Again, since normal adult cells aren’t built to divide forever like IPS cells, the same discussion above applies. If you’re seeing a trend here, you’re not the only one. In both instances, it’s our need to create cells that can be mass manufactured to satisfy a business model that creates the problem. How about adult stem cells like those used in the Regenexx procedure family? Adult stem cells are built to do what we’re asking them to do. They help repair tissue and then either differentiate into the bricks and mortar of the repair or they orchestrate the construction job and then disappear from the scene. Growing adult stem cells for short periods (like in the Regenexx-C procedure), still keeps the cells within the parameters of what happens in the body. Studies have shown no significant genetic abnormalities when adult stem cells are grown for short periods and more interestingly, when they are grown very long periods (months and months) and do pick up genetic abnormalities, they don’t form cancers, they just don’t work anymore. Our complications tracking data has also shown that using these short-term cultured stem cells in people poses less risks than the surgical procedures they help many patients avoid. This is consistent with the findings of others showing robust safety for cultured adult stem cells from bone marrow.
In summary, you can’t teach an old dog new tricks (I think that’s my third really bad turn of phrase). Trying to mass produce cells isn’t a good idea with our current state of knowledge. A better idea is using the patient’s own adult stem cells, which is the “customized” medicine long sought by physicians. While the business model may not be as good, it’s sure a heck of a lot safer for the patient.
Interesting study out this month showing that surgically removing part of a knee meniscus during arthroscopic surgery actually alters the way the knee works and leads to more cartilage to cartilage contact in the joint and thus likely more arthritis. To better understand this study, it helps to think of the knee meniscus as a spacer that keeps the two cartilage surfaces of the joint (the upper one on the femur bone and the lower one on the tibia bone) apart. Without this spacer, the two surfaces wear more on one another. Often after meniscus surgery to trim part of a torn meniscus, the meniscus begins to spit our of the joint, further reducing the ability of the spacer to protect the joint. All of this makes sense, as there’s noting about a smaller meniscus (after the torn parts have been cut out) that would make one think that the knee would be better off. This study confirms that changes in the way the knee works due to these menisectomy surgeries lead to more contact and wear and tear of the joint surfaces. This fits with other studies questioning why we’re still performing arthroscopic knee surgeries to treat a torn meniscus. In summary, less meniscus equals more arthritis and a knee that doesn’t work as well as the original equipment!