GAINESVILLE, Fla.—The millions of Americans who suffer from fibromyalgia live with a two-edged sword: excruciating pain, accompanied by the doubts of many who dismiss it as a made-up illness invented by a troubled mind.
But researchers at the University of Florida and elsewhere are beginning to piece together clues that reveal the physical basis of the puzzling syndrome that causes severe fatigue and aches, and has defied easy diagnosis.
UF scientists have found an abnormal central nervous system reaction in those with fibromyalgia-the body magnifies ordinary repetitive stimulation into an experience of crippling pain.
“This is particularly important because it has been unclear if fibromyalgia was just an imagined illness or a real syndrome,” said Dr. Roland Staud, an associate professor of medicine at UF’s College of Medicine who also is affiliated with the UF Brain Institute. “We now have good evidence that shows that it’s not a psychological abnormality, butthat there is a neurological abnormality present.”
Staud, who presented his research findings at the annual meeting of the American College of Rheumatology last November, recently was awarded a National Institutes of Health grant worth nearly $800,000 to continue his studies for the next four years. Donald Price, a UFprofessor of oral and maxillofacial surgery, and Charles Vierck, a UF professor of neuroscience, are collaborating on the research. Their goal is to develop a better understanding of the condition, with an eye toward improving diagnostic tests and treatments.
An estimated 3.7 million people in the United States – primarily women who are diagnosed during their 30s and 40s – have fibromyalgia, according to the NIH. A chronic illness with no known cure, its cause also is not known. Researchers have theorized that an injury to the central nervous system or an infectious agent might be responsible for triggeringit in people who have inherited susceptibility. Symptoms include persistent and widespread musculoskeletal pain, fatigue and tenderness in the neck, spine, shoulders and hips.
Staud and colleagues found the central nervous system abnormality byconducting a series of repetitive stimulation tests on people with thesyndrome as well as healthy research participants. The tests involved repeatedly placing warm plates on their hands and arms. The healthy participants felt the sensation but did not report it as pain.
For those with fibromyalgia, however, the sensation would magnify with each repetition into an experience of crippling and unbearable pain.
“When a sensation signal reaches the spinal cord, the signal can be omitted, changed or augmented,” Staud said. “If it is augmented, then something that is innocuous, such as pressure on the skin, can then be perceived as a painful stimulus.”
Jessica LeMay, one of Staud’s patients, has been battling fibromyalgia since 1993. The 30-year-old Lake City resident said the pain starts in one area and usually spreads, sometimes becoming overwhelming.
“I imagine if someone had taken a baseball bat and beaten me with it,that’s got to be what it feels like,” she said. “Depending on the day, I’ll just move out of the way if someone tries to touch me.”
The pain of fibromyalgia often interferes with a person’s working life.
“These are people who are diagnosed in their productive years. Many have personal or professional problems adjusting to the pain experience,” Staud said. “The illness makes some people feel dysfunctional because they can’t do the activities they once did.”
The condition can worsen from stress and inadequate sleep, Staud said. Because living with fibromyalgia often causes stress, and pain makes sleeping difficult, a vicious cycle develops.
LeMay said many people dismiss her condition, not understanding the “huge difference” between her severe fatigue and the healthy person’s occasional tiredness.
“When this fatigue would come about, it’s almost like a weight being dropped on you, and you can’t function anymore,” she said.
LeMay said she is hopeful that Staud’s research will lead to more effective treatment for fibromyalgia patients and better understanding by the general public.
“In our society, you either get better or you die, and fibromyalgiapatients don’t do that,” she said. “We don’t fit in the mold, so people don’t know what to do with us.”
Researchers in the U.K. report that non-restorative sleep is the strongest, independent predictor of widespread pain onset among adults over the age of 50. According to the study published in Arthritis & Rheumatology (formerly Arthritis & Rheumatism), a journal of the American College of Rheumatology (ACR), anxiety, memory impairment, and poor physical health among older adults may also increase the risk of developing widespread pain.
Muscle, bone and nerve (musculoskeletal) pain is more prevalent as people age, with up to 80% of people 65 years of age and older experiencing daily pain. Widespread pain that affects multiple areas of the body — the hallmark feature of fibromyalgia — affects 15% of women and 10% of men over age 50 according to previous studies.
Led by Dr. John McBeth from the Arthritis Research UK Primary Care Centre, Keele University in Staffordshire, this newly published population-based prospective study identified factors that increase the risk of the development of widespread pain in older adults. The team collected data on pain, psychological and physical health, lifestyle and demographic information from 4326 adults over the age of 50 who were free of widespread pain at the start of the study (1562 subjects reported no pain and 2764 had some pain). These participants were followed up three years later for the development of widespread pain.
Results show that at follow-up, 800 (19%) reported new widespread pain. The development of new widespread pain was greater in those with some pain at the start of the study; 679 (25%) of those with some pain and 121 (8%) of those with no pain at the start developed new widespread pain at three year follow-up.
Analyses determined that pain status, anxiety, physical health-related quality of life, cognitive complaint and non-restorative sleep were associated with increased risk of widespread pain development, after adjusting for osteoarthritis (OA). Increasing age was associated with a decreased likelihood of the development of widespread pain.
“While OA is linked to new onset of widespread pain, our findings also found that poor sleep, cognition, and physical and psychological health may increase pain risk,” concludes Dr. McBeth. “Combined interventions that treat both site-specific and widespread pain are needed for older adults.”
Lupus patients have been waiting a while for some good news. Only one drug, belimumab (Benlysta), has been FDA-approved for lupus in more than 50 years — and that happened back in 2011. Since then, scientists have been trying to develop additional therapeutic agents (and failing for various reasons). But research presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals (ACR/ARP) Annual Meeting in Atlanta suggests that a new lupus medication, anifrolumab, might have the potential to get approved and make its way to market.
The manufacturer, AstraZeneca, is expected to file for FDAapproval in 2020. It’s hardly a slam dunk: The company conducted two phase 3 trials on anifrolumab, and one of them did not hit its primary endpoint, though secondary endpoints suggested that the drug had benefits. The second phase 3 study, which was presented for the first time at the recent ACR/ARP meeting, yielded more consistently positive results.
“I’m optimistic and hopeful that this drug will be approved,” says Chronicwoman medical advisor Vinicius Domingues, MD. “We have one [phase 3] study that was technically negative but with a lot of positives because of the secondary endpoints, plus a second [phase 3] study that was all positive. Patients should know that this is promising.”
The first phase 3 trial was called TULIP 1 (Treatment of Uncontrolled Lupus via the Interferon Pathway). Last August, AstraZeneca reported that anifrolumab failed to meet its primary target in TULIP 1, which was a “statistically-significant reduction in disease activity… as measured by the SLE Responder Index 4 (SRI4) at 12 months.”
SRI4 is a composite score that is often used to measure disease activity in patients with systemic lupus during clinical trials. According to SRI4, anifrolumab was as flop: Patients who added the drug to their treatment regimen did not, on average, fare better than those who added a placebo.
However, secondary endpoints in TULIP 1 found that anifrolumab beat the placebo. Those secondary endpoints included a different composite score of disease activity, called BICLA (British Isles Lupus Assessment Group-Based Composite Lupus Assessment), as well as reduced reliance on corticosteroid drugs.
The results of TULIP 1 appear in the journal Lancet Rheumatology and were discussed at the 2019 ACR/ARP meeting.
TULIP 2, the second phase III study of anifrolumab, used BICLA as its primary endpoint — and met it. TULIP 2, which was also presented at the 2019 ACR/ARP meeting, found that the drug beat the placebo as far as BICLA was concerned. It also determined that patients using it had greater improvements in skin disease and decreased use of corticosteroids.
While it’s true that researchers deliberately switched to a primary endpoint that they were likely to meet when moving from TULIP 1 to TULIP 2, there’s no clear consensus among rheumatologists that SRI4 is “better” than BICLA. In fact, a 2014 study compared these two outcome measures and determined that either one could “likely be an optimal primary endpoint” in a given clinical trial.
According to Northwestern University rheumatologist Michael Putman, MD, reporting on the trials for RheumNow, the SRI4 requires 100 percent improvement in some domains, “whereas with the BICLA you can get a little better across the board.” That might be part of why one endpoint seemed to work and the other didn’t, he said.
Anifrolumab is a monoclonal antibody that inhibits type 1 interferons, proteins that are involved in inflammation. Some lupus patients (but not all) have a “high interferon gene signature.” Scientists are simultaneously developing a test that can be used to identify those individuals. “It can be used to help predict who may or may not respond to this drug,” says Dr. Domingues. “This is an example of precision medicine, and it’s how cancer is being treated nowadays.”
“There has been a case building for many years about the importance of interferons in the pathogenesis of lupus,” Timothy Niewold, MD, Judith and Stewart Colton Professor of Medicine and Pathology and Director of the Colton Center for Autoimmunity at the New York University School of Medicine, told the ACR Daily News. “One of the most exciting recent developments is that drug companies have created agents to target the interferon pathway. It’s been a rocky road, but there have been some positive results.”
If anifrolumab gets the green light from the FDA, patients who haven’t responded well to other lupus treatments — especially those who have a high interferon gene signature — might benefit by including it in their current drug regimen, says Dr. Domingues. (The drug would be an add-on, not a replacement.)
If the drug eventually gets approved, label specifics such as recommended dosing and warnings about side effects would be revealed at that time. In the TULIP 2 study, participants in the treatment group used 300 mg of anifrolumab via infusion every four weeks. Serious adverse events were rare and occurred more frequently among those in the placebo group. The most common side effect experienced by those using anifrolumab was shingles, which occurred in 7 percent of anifrolumab users.
“Giant cell arteritis requires ongoing management, but it does not necessarily require continuous treatment.”
In 2017, tocilizumab (Actemra), a biologic drug that inhibits interleukin-6 (IL-6), was FDA-approved for giant cell arteritis — an inflammation of the lining of the arteries. At the time there was sufficient research showing that tocilizumab was better than prednisone (a steroid) for helping many patients reach remission in GCA. Yet it was unclear whether those who had reached remission should stop taking the drug or if they needed to continue using it.
Now a new study, presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta, offers good news: A sizeable group of those who reached remission with tocilizumab were still in remission two years after stopping the drug.
The new study was an extension of an earlier 52-week study that led to tocilizumab’s FDA approval for giant cell arteritis. The drug is also approved for rheumatoid arthritis, juvenile idiopathic arthritis, and severe cytokine release syndrome.
More than 200 patients who had reached remission by using tocilizumab either once a week or every other week entered the post-marketing arm and were instructed to stop using the drug. According to their findings, 47 percent of those who had been previously taking tocilizumab weekly and 36 percent of those who had previously been taking it every other week remained in remission two years later.
Those who did experience flares were restarted on tocilizumab and/or given steroids. Those who resumed using tocilizumab (with or without a steroid) were once again able to reach remission.
“Giant cell arteritis requires ongoing management, but it does not necessarily require continuous treatment,” lead author John H. Stone, MD, MPH, told the ACR/ARP Daily News. “Patients should be started on tocilizumab as soon as they are diagnosed. The goal should be to get them off steroids as quickly as possible and maintain their response with tocilizumab.”
Some people with rheumatoid arthritis (RA) take a disease-modifying antirheumatic drug (DMARD) and/or a biologic and reach remission. Others try drug after drug after drug and never find one that’s effective — or that treats their symptoms without causing intolerable side effects. At the same time, other patients with active disease refuse to take the most powerful and effective medications on the market or can’t take them because of their medical history or personal risk factors that would make doing so dangerous.
While many scientists are continuing to explore better drug options, some are focused on developing new treatments that aren’t medications at all. One such experimental approach that’s gaining some traction is called vagus nerve stimulation, which entails using electrical impulses to stimulate the vagus nerve — the longest of the cranial nerves that stem from the brain.
The vagus nerve runs from the brain, through the face and neck, and down into the abdomen. It’s a key part of the autonomic nervous system, the division of your nervous system that controls functions you don’t have to think about, such as breathing, digesting food, and the beating of your heart. The vagus nerve is also the home of the inflammatory reflex, a pathway that appears to be crucial for detecting and modulating inflammation.
When something in your body gets injured or attacked by an invader (like a virus or bacteria), the vagus nerve helps decide how strong of an immune response the body should mount. When that response is appropriate, germs get killed off and injured tissue starts to heal. But when it’s too aggressive for the threat at hand — imagine trying to put out a small candle by holding it under a waterfall — you end up with chronic inflammation, which results in joint and tissue damage.
If you have an autoimmune condition, you already know that your immune system is far more revved up than it should be. In the case of RA, the immune system mistakenly tries to attack healthy tissue in the joints as well as in other organs. No one knows exactly what sets RA in motion, but experts do know that inflammatory substances called cytokines play an important role in causing tissue damage. Those cytokines include tumor necrosis factor (TNF) and interleukins (IL), among others.
Scientists now know that the vagus nerve has the power to reduce the production of them.
Vagus Nerve Stimulation vs. RA Medication: Same Targets, Different Approach
Many people with RA take drugs that target specific cytokines. Biologic medications such as etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade) target the ctytokine TNF, whereas anakinra (Kineret) targets IL-1 and tocilizumab (Actemra) and sarilumab (Kevzara) target IL-6.
But these drugs don’t work for everyone with RA. For these patients, stimulating the vagus nerve seems to be another way to reduce the production of cytokines that cause inflammation.
“The premise is that when you stimulate the vagus nerve it leads to the production of acetylcholine [a neurotransmitter], which binds to receptors on cells that secrete cytokines. When acetylcholine binds to those cytokine-producing cells, it inhibits them from producing TNF and interleukin-6,” says rheumatologist Mark Genovese, MD, a professor of medicine at Stanford University who conducted a pilot study on vagus nerve stimulation that was presented at the 2019 European Congress of Rheumatology (EULAR) conference.
In Genovese’s study, which was published as an abstract in the journal Annals of the Rheumatic Diseases, 14 people with RA who had tried and failed to respond to at least two medications had a small “MicroRegulator” — about the size of a nickel — implanted on the left side of the neck along the vagus nerve.
Although the primary goal of this small trial was to assess the safety of the device, half of patients who had impulses sent to the MicroRegulator once a day had significant improvements in their RA disease activity scores. A decrease in cytokine production was also measured.
A few adverse effects were reported, but all were temporary. Those included pain and swelling at the incision site as well as one patient who had temporary vocal cord paralysis.
Dr. Genovese is now helping SetPoint Medical, the company that is investigating vagus nerve science and sponsored the pilot study, design a much larger, multi-center clinical trial to learn more about whether vagus nerve stimulation can be used to treat RA, especially in people who don’t respond sufficiently to drugs.
Earlier studies, including another small trial that involved RA patients in Europe, similarly found that that implantable vagus nerve stimulator could be used to reduce TNF production and, in turn, inflammation.
While Dr. Genovese and SetPoint Medical are focused on implantable stimulators, other non-invasive approaches in this growing area of bioelectronic medicine are also being explored: One small study, published in the journal Bioelectronic Medicine this year, found that holding up a vibrational device to the ear could be used to stimulate the vagus nerve and inhibit the production of TNF, IL-1, and IL-6.
At the same time, researchers are trying to determine whether it’s possible to predict who is likely to respond well to RA medication and who’s apt to be a non-responder. One way to do that might be by testing vagal nerve tone: Low vagal tone has already been linked to more inflammation and a greater risk of autoimmune conditions.
Although more research is needed, RA patients with low vagal tone may turn out to be good candidates for vagus nerve stimulation. That’s the premise behind a medical device called ANS Neuroscan that’s being developed by Inmedix, says Vibeke Strand, MD, adjunct clinical professor in the division of immunology/rheumatology at Stanford University and a pharmaceutical and biotech consultant for companies including SetPoint Medical and Inmedix.
If ANS Neuroscan gets FDA clearance, rheumatologists might be able to use it as an in-office tool to help determine which patients are most likely to respond to biologics and who might fare better on an emerging therapy such as vagus nerve stimulation. This device provides information about vagal tone by measuring heart rate variability (as do electrocardiograms and a number of apps and gadgets like the Apple Watch).
Dr. Strand also notes that while patients who are found to have low vagal tone might very well benefit from vagus nerve stimulation, electrical impulses aren’t the only way to do it. You might be able to improve your vagal tone on your own by learning some specific breathing techniques or employing other mind-body strategies, though substantial training is likely to be involved.
“There’s a lot of stress associated with having rheumatoid arthritis, or any autoimmune disease, and that’s probably leading to some of the immune system over-activity and the autoimmune response” as modulated by the vagus nerve, says Dr. Strand.
The vagus nerve, she explains, is integral to the mind-body connection. It’s a major route by which messages travel between the brain and the gastrointestinal tract (gut-brain axis), which is why vagus nerve stimulation has also gained attention as a treatment for psychiatric and digestive disorders.
“The autonomic nervous system is part and parcel of our immune response,” says Dr. Strand. “It takes a little time for some people to wrap their heads around that.”
If ongoing and future studies are positive, vagus nerve stimulation might one day become a viable option for RA patients who don’t respond to medication, can’t take it, or don’t want to, says Dr. Strand. Some new research is also examining whether electrical nerve stimulators might be used in conjunction with drug therapies to boost their effectiveness, says Dr. Genovese.
While all this might sound a bit futuristic, vagus nerve stimulators are already on the market — just not yet for RA. Implantable stimulators have been FDA-approved for patients with drug treatment-resistant epilepsy and depression since 1997, and there’s an FDA-cleared non-invasive device aimed at people who get migraine attacks and cluster headaches. In addition to RA, vagus nerve stimulation is being investigated for a wide range of potential applications including inflammatory bowel disease, bipolar disorder, and Alzheimer’s disease.
Will rheumatoid arthritis patients soon be able to make use of a similarly FDA–approved implant or non-invasive device? Stay tuned, as the results of upcoming trials are expected in the near future.
The anti-malarial drug lowers cholesterol and blood sugar makes blood less sticky, which is good for reducing blood clots and heart attack risk.
If you take the anti-malarial drug hydroxychloroquine (Plaquenil) as part of your treatment for lupus or rheumatoid arthritis (RA), you may be getting cardiovascular protection as an added bonus.
That’s welcome news because it’s estimated that about half of lupus patients experience heart complications, and heart attacks occur at younger ages in lupus patients than in the general population. Even as young adults, black and Hispanic women with lupus often have plaque build-up in their arteries that hikes their risk of heart attack. And experts have long known that people with RA are more likely to develop heart disease, even if they don’t show signs of clogged arteries: inflammation from arthritis disease activity is thought to be the link.
Because hydroxychloroquine (HCQ) has been associated with lower levels of cholesterol, blood sugar, and the tendency of blood to clot — all cardiovascular risk factors — researchers looked at the association between HCQ use and the occurrence of heart attacks, strokes, and blood clots (in lungs or deep veins). The results were presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals annual meeting in Atlanta.
Using a health database that covers the entire population of British Columbia in Canada, researchers compared lupus and rheumatoid arthritis patients who had experienced a cardiovascular event with up to three matched patients who did not have a cardiovascular incident. Most of the patients were female (64 percent) and their average age was 74. In total, researchers studied 532 lupus cardiovascular cases and 1,249 controls, as well as 9,736 RA cardiovascular cases and 28,720 controls.
HCQ use was categorized by the most recent date covered by a prescription and divided into those currently using the medication (within last month), those who recently stopped using it (used within 30 to 365 days), those who stopped using HCQ more than a year previously, and those who had never taken it.
After controlling for such other factors as kidney disease and the use of glucocorticoids, disease-modifying anti-rheumatic drugs, and heart disease medication, lupus and RA patients currently using HCQ were 17 percent less likely to have a heart, stroke, or blood clot.
In contrast, those who had discontinued HCQ within the last year were 8 percent more likely to have one of the cardiovascular events.
When people stopped using HCQ more than a year ago, the risk of cardiovascular events was no different than those who had never been prescribed HCQ.
In another hydroxychloroquine study presented at the meeting, Johns Hopkins researchers looked at blood levels of HCQ in lupus patients who developed a blood clot (including heart attacks and clot-caused strokes). They found that patients with the highest levels of HCQ in their bloodstreams were the least likely to have developed a clot.
The researchers cautioned that following the suggestion of the American Academy of Ophthalmologists to reduce HCQ doses in an effort to prevent damage to the retina (which occurs in about one out of 5,000 patients taking HCQ for more than five years, according to Johns Hopkins), may also reduce or eliminate the benefit of HCQ in preventing blood clots.
If you’re taking hydroxychloroquine and are concerned about your dosage and how it may affect your heart disease risk or the odds of vision problems, talk to your rheumatologist and ophthalmologist to understand your risk factors and make the right decision for you.
Screening is important because silent hepatitis B and Cinfections can spring to life when you start biologics or new synthetic DMARDs.
Before you start taking a biologic drug or one of the new targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), several screening tests are recommended. These include tests to see whether you have hepatitis B or C in your body that isn’t causing symptoms but might be reactivated after you start these powerful immune-suppressing drugs.
But there’s a big gap between what’s recommended and what’s really happening, as a new study reveals that fewer than one in four patients in a national registry received hepatitis screening before starting these medications.
“I think that we all believe that we are doing an excellent job taking care of our patients, but what we found is that there is a gap of care around screening for these infections,” Gabriela Schmajuk, MD, of the University of California, San Francisco, told Healio Rheumatology. Dr. Schmajuk was senior author of the new study, which was presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta.
The researchers looked at electronic health records from 23,597 patients (average age 57, 72 percent female) being treated at 196 different practices participating in the Rheumatology Informatics System for Effectiveness national registry. Each received their first prescription for a biologic or new synthetic DMARD in 2017, with the majority (63 percent) starting a tumor necrosis factor inhibitor.
Prior to the first prescription, 77 percent were not screened for hepatitis B virus (HBV) and 86 percent were not screened for hepatitis C virus (HCV). Only 6 percent of patients were fully screened for HBV, including both HBV surface antigen and HBV core antibody, prior to their first prescription. Another 17 percent had received one of the tests. Only 14 percent of patients received complete testing for HCV prior to their first prescription.
Of the patients who were fully screened, 83% had screening completed before receiving their first prescription, and a total of 97% had completed screening within 60 days of receiving their prescription.
“We actually looked to see, among the patients who were screened, how many had a positive test, and we found a rate of about 2 to 3 percent, so it is not insignificant,” Dr. Schmajuk told Healio Rheumatology. “If we can prevent one of those people from reactivating, that is going to save all of the money that we spent in screening them.”
Reactivation of HBV may lead to a hepatitis flare, liver failure, and sometimes even death, so patients who screen positive for the virus are often treated with an antiviral medication to prevent reactivation and its complications. HCV reactivation can also lead to hepatitis, but it may not be as severe as that caused by HBV reactivation.
The researchers acknowledge that their data, which can only capture screening entered into electronic health records at the rheumatology practices, could be missing hepatitis screening that was only noted in writing in the patient chart or conducted elsewhere and faxed to the practice, not making it into the electronic record.
Pre-medication screening percentages differed wildly between practices, with 0 percent to 63 percent of patients screened for HBV and 0 percent to 80 percent of patients screened for HCV.
If you’re not sure whether you have been screened for hepatitis B or C and you’re starting a biologic medication make sure you ask your health care provider.
No one knows what causes fibromyalgia but some experts believe that stress may be a common trigger, especially in people who are susceptible to this chronic pain condition for physiological reasons. Now a new study adds support to the theory that psychological stress might increase the risk as well as lead to worse symptoms among those who have fibromyalgia.
Researchers at the Cleveland Clinic enrolled 593 fibromyalgia patients and surveyed them about their symptoms and history of abuse. Nearly 38 percent of fibromyalgia patients said that they had been physically and/or sexually abused at some point.
According to this study, patients who had a history of abuse were also more likely than those who had not been abused to report more severe fibromyalgia symptoms. Patients with a history of abuse had higher pain disability index scores, more generalized weakness, and had visited doctors more frequently.
Those who had been abused were also more apt to be seeing a psychiatrist and to have a drinking problem or a personal history of alcohol abuse.
“Our results suggest that stressors such as abuse have a wide range of detrimental effects on [fibromyalgia,]” the authors concluded. “We recommend that abuse should be inquired about in all patients evaluated for [fibromyalgia] as this may give more clarity to the nature and severity of the [fibromyalgia] presentation and prompt the need for psychological interventions.”
Osteoarthritis is the most common and well-known type of arthritis. It’s largely a wear-and-tear form of arthritis that happens as a result of damage to or overuse of a joint, usually over a long period of time. About 30 million Americans have osteoarthritis. You can also have osteoarthritis at the same time as other kinds of arthritis that are inflammation- or immune-related, such as rheumatoid arthritis, gout, psoriatic arthritis, or ankylosing spondylitis.
In osteoarthritis, the cartilage — the smooth, rubbery connective tissue on the end of bones that cushions the joint, helping bones move smoothly and easily — wears down until the bones are painfully rubbing against each other. This cartilage breakdown also causes the bones in the joint to undergo changes, including the appearance of bone spurs. Bone spurs are bony projections that develop alone the edges of bones in the joints, also knowns as osteophytes. Tendons, ligaments, and muscles are also affected and there can be inflammation in the joint.
“OA isn’t just about the cartilage,” says Lisa A. Mandl, MD, MPH, a rheumatologist at Hospital for Special Surgery in New York City, who specializes in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and osteoarthritis. “It is a disease of the whole joint. The ligaments are weak, the tendons are frayed, the muscles are weak.” This generally happens slowly and worsens over time. Weight-bearing joints like the hips, knees, and spine are most vulnerable to osteoarthritis. Other common spots are the hands, wrists, and shoulders.
Osteoarthritis is often thought to be “less serious” than autoimmune forms of arthritis like rheumatoid arthritis. While that may be the case to a certain extent (the systemic inflammation an autoimmune illness like RA can impact organs and systems throughout your body), OA can take a significant toll on how you feel and function. In fact, according to a new study, published in the journal Arthritis & Rheumatology, the “disease burden” is similar among OA and RA patients at the time of diagnosis; but six months into treatment, RA patients often tend fare better. This may be because RA has many disease-modifying drug options, while OA’s treatments tend to focus more on symptom management.
Many experts believe that anyone who lives long enough will eventually develop some degree of osteoarthritis in some joints. Still, osteoarthritis isn’t caused by any one specific risk factor. Rather, certain risk factors, as outlined below, make you more susceptible to developing osteoarthritis in one or several joints.
Age is the strongest non-modifiable risk factor for OA, says Dr. Mandl. Approximately 14 percent of adults aged 25 and older have symptomatic OA of at least one joint while at least 34 percent of adults aged 65 and older have OA. Worldwide estimates are that 10 percent of men and 18 percent of women aged 60 years old and over have symptomatic OA.
The reason behind this risk for OA increasing with age aren’t fully known. Possible causes could be loss of normal bone structure, overuse of joints over time, and increased stiffness of ligaments and tendons. “It’s just general life experience over time,” says Christopher Collins, MD, an attending rheumatologist and associate program director of the rheumatology division at MedStar Washington Hospital Center and an associate professor of medicine at Georgetown University Medical Center in Washington, D.C. “It’s like a car. After a while, some of the parts start to wear down.”
Sex plays a role in osteoarthritis risk. Yes, both women and men get OA. But it’s more common in men until age 45. After that age, osteoarthritis is more common in women, according to the National Institute on Aging.
The risk of OA by sex also depends on the joints. Knee and hand osteoarthritis are more common in women than men; the frequency of hip OA is the same in women and men, says Dr. Mandl. She says that it’s unknown for sure why this happens. It may be that force hits the knee and body differently in women compared to men. Previously, researchers had thought that it was because men and women experienced stress on the joints at different ages.
Newer research has found a connection between estrogen and joint health. A report in the Journal of Mid-Life Health found that menopause is associated with the onset and progression of OA in women, which may explain why OA affects older women more commonly than older men. Still, Dr. Mandl stresses that this link is unclear and hard to prove.
An injury related to playing sports, a fall, a vehicle accident, or other physical trauma can cause OA in adults of any age. Sports-related knee trauma, such as a strain or tear of the ACL (anterior cruciate ligament), has been linked to an increased risk of developing knee OA, research shows. In fact, Dr. Mandl says that half of people who have ruptured their ACL will have severe OA within a decade. In fact, any kind of surgery to the knee increases the risk of OA down the road, she says. Even joint-related injuries that happened years ago and seemingly healed can increase your risk of developing osteoarthritis. Common injuries that can lead to OA include torn cartilage, dislocated joints, and ligament injuries.
The onset of osteoarthritis can also be linked to a repetitive activity that damages the joints like operating a jackhammer with your hands or sitting on your knees while laying bricks, says Mark C. Genovese, MD, the James W. Raitt professor of medicine and director of the rheumatology clinic in the division of immunology and rheumatology at Stanford University Medical Center in Palo Alto, California.
Your weight is the biggest modifiable risk factor for developing osteoarthritis, says Dr. Mandl. Excess weight places additional stress on weight-bearing joints, especially your knees and hips, she says. A report in Obesity Reviews found that losing 10 pounds can help manage OA and lead to improvement in symptoms, pain, function, and quality of life.
“Even losing five pounds can make a difference,” says Dr. Mandl. “The heavier you are, the more likely you are to develop knee OA and for it to progress and become more severe. It’s never too late to lose weight.” Fat tissue also produces proteins that can cause harmful inflammation in and around your joints. Being overweight also can speed the progression of the disease on weight-bearing joints like knees, feet, and lower back, says Dr. Genovese.
People who do certain activities for hours may be more likely to develop stiffness and joint pain. Activities include repetitive bending, kneeling, and squatting. Joints commonly affected by this include the hands, knees, and hips. The mechanism for the association remains unclear, though joint loading (force on a wearing-bearing joint during activity) and repetitive damage may be a factor. A paper in the journal Best Practice & Research in Clinical Rheumatology found — not surprisingly — that doing heavy manual work is a risk factor of osteoarthritis. Researchers from the United Kingdom found that those with the highest risk have worked in agriculture and farming for 10 or more years.
OA tends to run in families, especially if you have genetic joint defects. You’re more likely to have osteoarthritis symptoms if your parents, grandparents, or siblings have the condition. Researchers don’t know why OA runs in families. While genetics are a risk factor, no one gene has been identified as causing the condition. “We believe that there is a large genetic component with the development of OA,” says Dr. Genovese. “But there is not a single gene association the way you might see with other diseases.”
Though they’re not common, medical conditions that involve bleeding near a joint can cause osteoarthritis to worsen or new symptoms to develop. If you have hemophilia (where blood doesn’t clot normally) or avascular necrosis (the death of bone tissue due to a lack of blood supply), you may have symptoms associated with OA. “Blood is irritating and really destructive to the joint,” says Dr. Mandl.
If you have other forms of arthritis, such as gout or rheumatoid arthritis, you’re more at risk for developing osteoarthritis too. RA is an autoimmune disease in which your immune system mistakenly attacks the joints. This triggers inflammation that thickens the synovial tissue lining the inside of the joint, causing swelling and pain in around the joints. Gout is a painful and acute onset of arthritis caused by the buildup of uric acid (a normal waste product in your body) in the blood. When uric acid is elevated in the blood, it can accumulate in your joints and trigger an inflammatory response that causes severe pain and swelling.
People born with certain diseases or health problems are more likely to develop OA. Examples include increased joint laxity (being double-jointed), some dysplasias (abnormal growths of bone and cartilage), and Paget’s disease (a type of bone inflammation).
Other conditions that can lead to OA include peripheralneuropathies (nervous system disease) and neuromuscular disorders that put abnormal stress on the joint. Certain metabolic diseases like diabetes and hemochromatosis (where your body has too much iron) make you prone to OA as well as bone deformities like those born with malformed joints or defective cartilage.
If you suspect your joint pain or other symptoms could be OA, and you have some osteoarthritis risk factors (or even if you don’t), see your primary health care provider. You may need a referral to a specialist such as a rheumatologist or orthopedist for further testing and treatment.
As the temperature increased, so did the risk of rash, joint inflammation, kidney problems, and other lupus symptoms.
Shifts in weather patterns have long been associated with a variety of health ailments, from seasonal allergies to migraine and joint pain. Now a new study suggests that changes in the outdoor environment may make people who have lupus more susceptible to flare-ups of specific symptoms.
The study, presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta, analyzed data on 1,628 patients with lupus who had checkups between 1999 and 2017 as well as environmental and atmospheric data from the U.S. Environmental Protection Agency. The goal: to determine whether the environmental weather conditions 10 days before a checkup would correlate to changes in patient symptoms.
According to the authors, “there is a strong association between changes in atmospheric and environmental variables 10 days prior to patient visit and organ-specific lupus activity at the visit.”
Although they did not find a connection to systemic flares that impact all organs, they determined that certain environmental factors were strongly linked to flares of specific symptoms: As the temperature increased, so did the risk of rash, joint inflammation, kidney problems, serositis (inflammation of smooth tissue membranes), and hematologic problems such as anemia and low white blood cell count.
Windy conditions were also apt to lead to a spike in hematologic problems, plus an increase in neurological and pulmonary symptoms. Reports of joint inflammation and serositis increased in more humid weather, and an increase in air pollution (fine particulate matter) correlated to an uptick in rash, joint, serositis, and hematologic flares.
Although more research is needed to confirm the results, “these findings are the first step to vindicating the great majority of lupus patients who are convinced that their disease is influenced by weather changes and who inspired this research,” lead study author George Stojan, MD, assistant professor of medicine at Johns Hopkins Lupus Center, said in a press release.
