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The American College of Physicians (ACP) has published an update to the 2017 version of its recommendations regarding newer pharmacologic treatments for type 2 diabetes, including glucagon-like peptide-1 (GLP-1) agonists, sodium-glucose cotransporter-2 (SGLT-2) inhibitors, dipeptidyl peptidase-4 (DPP-4) inhibitors, and long-acting insulins. The full update was published in Annals of Internal Medicine.
In 2017, the ACP recommended metformin as an adjunct to lifestyle modifications to improve glycemic control among adults with type 2 diabetes. However, 16% of adults with type 2 diabetes have inadequate glycemic control, which is most prevalent among Black and Hispanic adults compared with White adults.
To assess the effectiveness of type 2 diabetes treatments in reducing all-cause mortality, cardiovascular morbidity, and chronic kidney disease (CKD) progression, the Clinical Guidelines Committee of the ACP conducted a systematic review and network meta-analysis of randomized controlled trials with a duration of at least 12 months.
Critical outcomes included all-cause mortality, congestive heart failure (CHF), major adverse cardiovascular events (MACE), myocardial infarction alone, progression of CKD, serious adverse events, and severe hypoglycemia. The ACP also assessed patient values and preferences for new treatments, as well as the costs and economic burden of care.
Clinical Considerations
The ACP recommendations apply to nonpregnant adults with long-standing type 2 diabetes and a mean hemoglobin A1c (HbA1c) of approximately 8%. Because evidence was insufficient to differentiate between patients with and without cardiovascular disease or CKD, these recommendations apply to patients regardless of cardiovascular disease or CKD status.
Metformin and lifestyle modifications should remain the first line of treatment for managing type 2 diabetes. When considering additional therapy, clinicians should weigh benefits vs harms, cost of medications, and individual patient factors such as comorbid conditions and glycemic control targets.
"
Benefits and harms of additional pharmacologic treatment beyond the initial add-on treatment are unknown (for example, a patient who receives metformin plus an SGLT-2 inhibitor but in the future receives an additional GLP-1 agonist).
Glycemic control targets should include considerations for hypoglycemia risks, life expectancy, diabetes duration, comorbidities, capacity for self-monitoring, and access to resources. The ACP recommends glycemic control target values between 7% and 8% for most adults with type 2 diabetes. For adults with HbA1c levels below 6.5%, clinicians should attenuate pharmacologic treatments.
SGLT-2 Inhibitors and GLP-1 Agonists
The ACP recommends prescribing an SGLT-2 inhibitor or GLP-1 agonist as an adjunct to metformin and lifestyle modifications to improve glycemic control among adults with type 2 diabetes. Among patients receiving metformin and SGLT-2 inhibitor or GLP-1 agonist combination therapy, blood glucose self-monitoring may be unnecessary.
Specifically, the ACP recommends SGLT-2 inhibitors to reduce the risks for all-cause mortality, MACE, progression of CKD, and hospitalization due to CHF. To reduce the risk for all-cause mortality, MACE, and stroke, GLP-1 agonists are recommended.
In the cost-effectiveness analysis, the ACP identified no significant differences between SGLT-2 inhibitors and GLP-1 agonists.
According to the ACP, SGLT-2 inhibitors should be prioritized for patients with type 2 diabetes and CHF or CKD, whereas GLP-1 agonists should be prioritized for patients with type 2 diabetes and an increased risk for stroke or total body weight loss goals.
The ACP also recommends the reduction or discontinuation of sulfonylureas or long-acting insulin treatments when adding an SGLT-2 inhibitor or GLP-1 agonist to a patient’s treatment regimen. Compared with SGLT-2 inhibitors and GLP-1 agonists, sulfonylureas and long-acting insulins were less effective for reducing all-cause mortality and morbidity.
DPP-4 Inhibitors
The ACP recommends against prescribing a DPP-4 inhibitor as an adjunct to metformin and lifestyle modifications to improve glycemic control among adults with type 2 diabetes.
In their analysis, the ACP identified no differences in the critical outcomes between patients prescribed adjunctive DPP-4 inhibitors and those who received usual care. Compared with GLP-1 agonists, DPP-4 inhibitors likely increase the risks for all-cause mortality, hospitalization due to CHF, and MACE.
“Benefits and harms of additional pharmacologic treatment beyond the initial add-on treatment are unknown (for example, a patient who receives metformin plus an SGLT-2 inhibitor but in the future receives an additional GLP-1 agonist),” the ACP concluded. “Further, clinical evidence on patient mortality, morbidity, and hospitalizations and economic evidence are lacking for use of SGLT-2 inhibitors and GLP-1 agonists as initial treatment for patients with type 2 diabetes.”
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This month, we look at a reproductive endocrinology case that discussed wrongful birth vs wrongful life lawsuits. In it, a New York court had to decide whether the statute of limitations runs from the act of negligence or the birth of the child.
Facts of the Case
Mr and Mrs. F were desperate to have a baby. The couple had been trying to conceive naturally and finally decided to seek medical help. They made an appointment with Dr C, the head physician at a large reproductive endocrinology practice, to discuss in vitro fertilization (IVF). Dr C explained the IVF process, telling the couple that the practice screened egg donor candidates for genetic diseases and other conditions. However, he did not disclose which specific conditions he screened for or the reasoning behind the screening process.
The couple were put on the waiting list for an egg donor. Months later, they were matched with a donor, whom they accepted. Mr and Mrs. F signed a consent form agreeing to go ahead with the IVF procedure. The consent form contained language stating that the prospective parents “understand that the risk of major birth defects following the use of donor eggs appears to be the same as in the general population.”
In January, 2 embryos were implanted into Mrs. F. The embryos were produced by fertilizing donated ovum with Mr F’s sperm. Much to the couple’s delight, they were pregnant soon after. Mrs. F’s final appointment with Dr C was in March. In September, Mrs. F gave birth to twin boys.
The following February, Dr C received information that Mr and Mrs. F’s egg donor might have a genetic mutation. He had the donor come in to be tested for a chromosomal abnormality known as Fragile X, which can produce intellectual impairment and other disabilities, particularly in boys.
The donor turned out to be a carrier for the condition. She had not been tested for it prior to donating eggs to Mr and Mrs. F. That May, Dr C called Mrs. F and notified her that the egg donor was a Fragile X carrier. Mr and Mrs. F had their sons tested for the condition and learned that one of them had the full mutation.
A year and a half later, Mr and Mrs. F sued Dr C and his practice for a dozen causes of action, including medical negligence, breach of contract, and negligent misrepresentation.
The physician retained an attorney who moved to dismiss half of the claims. Specifically, the attorney asked to dismiss any claims made on behalf of the impaired child. The court granted the defendant’s request, holding that such claims would amount to a “wrongful life” claim that is not recognized in New York. Parents cannot bring a claim on behalf of the child arguing that the child would have been better off not being born. Parents can, however, bring a claim for wrongful birth, if they can establish that the child would not have been conceived but for the defendant’s malpractice or that the malpractice deprived them of the opportunity to terminate the pregnancy.
The court dismissed the wrongful life claims but allowed the wrongful birth claims to proceed. At this point, the physician moved to have the remining claims dismissed. The physician argued that the statute of limitations for a medical malpractice case is 2½ years, and that the last time he had treated the patient was over 2½ years earlier. Thus, the physician claimed, the lawsuit was barred by the statute of limitations. The parents argued that the statute of limitations should run from the birth of the child — not the last time the mother was treated by Dr C. The case went to the state’s highest court for a decision on this issue.
Legal Background
The court noted that in 1978 it recognized a new cause of action allowing parents to recover for the extraordinary care and treatment expenses resulting from the birth of a child with a disability (ie, wrongful birth). However, the claim is restricted to the following instance: The plaintiffs have to show that, if it weren’t for the defendant’s breach of duty to advise the plaintiffs, they would not have been required to assume the extraordinary financial expenses. Parents bringing this kind of action can only recover for the increased financial obligation that they incurred by having a child with a disability. Parents cannot seek compensation for emotional damage or the ordinary costs of raising a healthy child.
"
Wrongful birth claims, however, are designed to provide parents with financial compensation to offset the costs involved with raising a child with birth defects. In such cases, the statute of limitations does not begin to run until the birth of the child.
“The question now before this Court is when this ‘extraordinary expenses’ cause of action accrues — and consequently when the statute of limitations begins to run,” the court noted in its decision. Dr C argued that it was the date of the malpractice, whereas Mr and Mrs. F argued that it was at the date of the child’s birth.
“Plaintiffs allege that, by failing to take steps to detect that the egg donor was a carrier for Fragile X and therefore that the embryo may have had the Fragile X trait, defendants left the parents in an uninformed state as to whether to avert pregnancy or birth — and the associated costs resulting from birth. Given the nature of these allegations, it follows that until the alleged misconduct results in the birth of a child, there can be no extraordinary expenses claim,” the court held in its decision.
“Prior to a live birth, it is impossible to ascertain whether parents will bear any extraordinary expenses. Due to these unique circumstances, the cause of action accrues upon the birth of an infant with a disability,” the court declared. The court allowed the case to stand against the physician.
Protecting Yourself
It’s important to know the difference between a wrongful birth claim and a wrongful life claim. Less than a handful of states allow wrongful life claims. A wrongful life case would be filed on behalf of the child with a disability, with the argument: Were it not for the negligence of the defendant, the plaintiff would not have been born. Courts have traditionally been very reluctant to award damages in these types of cases, and the vast majority of jurisdictions do not allow such claims.
Wrongful birth claims, however, are designed to provide parents with financial compensation to offset the costs involved with raising a child with birth defects. In such cases, the statute of limitations does not begin to run until the birth of the child.
Dr C’s failure to screen for Fragile X affected more than just Mr and Mrs. F. A second couple with a very similar case consolidated their legal matter with this case for that reason. The second couple used the same doctor and egg donor and subsequently gave birth to a son, who had the Fragile X abnormality. Dr C should have (1) told his patients exactly which conditions he was screening the donors for, and (2) used a more comprehensive screening panel.
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In the demanding and emotionally-charged field of health care, physicians often find themselves at the forefront of providing care and support to patients and their loved ones. While empathy and compassion are essential qualities in this profession, the constant exposure to suffering and the pressure to deliver optimal care can take a toll on the emotional well-being of health care professionals. These concerns are particularly true in certain environments like palliative care settings.1 In addition, intense workloads and limited resources during the COVID-19 pandemic further highlighted the mental health crisis facing many health care workers.2
A specific form of psychological distress known as compassion fatigue has emerged as an important topic in need of further research and attention. Compassion fatigue is a state of emotional exhaustion that can reduce your capacity for empathy,1 ultimately putting patient care at risk. To remain effective, health care professionals need strategies to identify the signs of compassion fatigue and alleviate its symptoms before the cumulative stress of work takes over.
How to Recognize Compassion Fatigue
Compassion fatigue is a psychological and physical state that occurs when health care professionals become emotionally drained from their efforts to care for patients. It is often a result of prolonged exposure to patients' suffering, traumatic events, or the inability to alleviate their pain. Experts have defined compassion fatigue as a combination of secondary traumatic stress and burnout.1 It may be viewed as, “the phenomenon of stress resulting from exposure to a traumatized individual rather than from exposure to the trauma itself.”3
As physicians experience increased levels of stress and burnout, they may feel emotionally detached and helpless, losing their sense of purpose. Some warning signs you shouldn't ignore include:
- Apathy and cynicism: A growing sense of pessimism may develop, affecting interactions with patients, colleagues, family, and friends.
- Decreased job satisfaction: Compassion fatigue often leads to frustration and dissatisfaction with one's profession, increasing absenteeism and making physicians question their career choices.3
- Emotional withdrawal: Physicians may emotionally detach themselves from patients and colleagues, leading to numbness or indifference towards their work.
- Physical exhaustion: Feeling constantly tired, irritable, or experiencing sleep disturbances, along with a lack of enthusiasm for work, are signs of compassion fatigue.
- Reduced empathy: A once empathetic physician may find it challenging to connect with patients emotionally, leading to a decline in the quality of care provided.
Studies suggest that the greatest mental health concerns for health care providers during the pandemic included insomnia, anxiety, depression, post-traumatic stress disorder, and stress.2 Untreated compassion fatigue and mental health issues can lead to unhealthy coping strategies, including drug and alcohol use disorders.3
Physicians need to remember that their well-being matters. No one is immune to the weight of such significant responsibility. Getting lost in caring for others isn't sustainable. In fact, doing so may compromise patient care, resulting in widespread negative consequences both personally and professionally.2
Preventing Compassion Fatigue
Physicians can use proactive strategies to combat compassion fatigue that promote self-care and emotional resilience. Physicians must prioritize self-care by taking regular breaks, engaging in hobbies, maintaining a healthy work-life balance, and setting boundaries to protect their well-being. Practicing mindfulness and meditation techniques can help physicians stay present and grounded.4
The opposite of compassion fatigue, referred to as “compassion satisfaction” describes pleasure experienced from relieving patient suffering and enjoying a positive work environment.1 Perhaps one of the best ways to avoid compassion fatigue is by focusing on the satisfying aspect of work, taking time to document and reflect on the positive effects of your efforts, even if they seem small in the larger context of a patient’s eventual outcomes.
Seeking professional counseling or therapy can be immensely beneficial in processing emotional challenges and building coping mechanisms. Counseling can be an opportunity to share small wins and talk through traumatizing experiences. In addition, open communication and sharing with colleagues can create a supportive environment where physicians can seek guidance and understanding. Hospitals and medical institutions should provide training and education on compassion fatigue to help combat this increasing problem for physicians around the world.5
More experienced physicians who take time for their mental wellness can positively impact the culture of medicine by setting a healthier example for students and residents entering the field. As research, awareness, and resources related to compassion fatigue increase, the stigma of mental health care should continue to decrease.5
Alleviating Compassion Fatigue
Despite best efforts, compassion fatigue in health care can seem unavoidable. Physicians must first acknowledge and accept that they are experiencing compassion fatigue. Denying or ignoring these feelings can exacerbate the problem.
It is crucial to lean on support systems, whether it be friends, family, colleagues, or professional counselors. Supervisors can also be a supportive resource. Talking about emotions and seeking understanding can help reduce the burden.1 In addition, therapy can help physicians understand their boundaries and limitations, including the fact that it’s not always possible to change a patient’s outcome or circumstances.1 To shift the focus to compassion satisfaction, physicians must find ways to see the rewards and accomplishments in their work.1
Long shifts and physical exhaustion often make it harder to weather the demands of working in health care. Therefore, time off to rest is vital. Physicians should not hesitate to use their leave entitlements when needed. Time off is critical to staying engaged and should be viewed as a necessary aspect of the job. It should also be used wisely as an active time to rejuvenate. In addition, activities that promote relaxation and joy, such as physical exercise, fun hobbies, or spending time in nature, can help reduce stress levels so you can bring your best self to work.1
Resources for Physician Self-Care
Many health care providers face unrealistic expectations, traumatic experiences, and a challenging work environment. Fortunately, more institutions and organizations recognize and provide resources to address burnout and compassion fatigue. If you're struggling with compassion fatigue (or simply trying to prevent it), you may want to seek out some of the following resources:
- Employee assistance programs (EAPs): Many health care facilities offer EAPs that provide confidential counseling and support services for employees facing emotional challenges.
- Peer support groups: Some medical institutions organize support groups for physicians to share their experiences, struggles, and coping strategies in a safe and understanding environment.
- Therapy: Many medical societies and organizations provide access to professional counseling services specialized in supporting health care professionals.
- Wellness workshops and retreats: Hospitals and medical associations often conduct workshops and seminars on stress management and promoting physician well-being.
Helping Yourself to Help Others
Compassion fatigue is a significant challenge faced by health care professionals, particularly physicians, who dedicate their lives to caring for others. By recognizing the signs of compassion fatigue, taking preventive measures, and utilizing available resources, physicians can safeguard their emotional well-being and continue providing exceptional patient care.
Acknowledging and addressing compassion fatigue is not a sign of weakness but a demonstration of strength and dedication to your profession and patients. Unfortunately, despite an increased awareness of physician burnout and compassion fatigue, there’s still no official guidelines for treatment.5 More research into this common phenomenon can help promote the development of more effective interventions.3 By promoting a culture of understanding, and support, health care institutions can contribute to a healthier and more resilient workforce, improving physicians’ lives and patient outcomes.
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Exercise has long been considered a core component of conservative treatment for osteoarthritis (OA).1 Health organizations — including the Arthritis Foundation,2,3 Centers for Disease Control and Prevention,4 American College of Sports Medicine (ACSM),5,6 and the Osteoarthritis Action Alliance7 — have strongly encouraged individuals with OA and those at risk of developing OA to stay regularly active, advertising the many benefits of exercise for people with this condition.
How exactly does exercise benefit people with OA? What exactly is happening at the joint and molecular level to achieve these benefits?
Exercise Increases Joint Range of Motion
As mentioned in a previous Rheumatology Advisor article, OA results in neuronally-mediated pain responses that promote natural behaviors, such as aversion to and avoidance of pain-inducing activities and self-imposed immobilization in an attempt to thwart further pain exacerbation. Though counterintuitive, immobilization can further promote joint stiffness and changes in viscosity of the synovial fluid inside the joint.
Normal joint synovial fluid contains high concentrations of hyaluronan,8,9 which plays a key role in cartilage biomechanics. Hyaluronan is a polysaccharide that increases joint lubrication and synovial viscosity into the synovial cavity.8 The presence of sufficient amounts of hyaluronan in the synovial fluid reduces the coefficient of friction between the articular cartilages during motion of the joint.10,11
"
Though counterintuitive, immobilization can further promote joint stiffness and changes in viscosity of the synovial fluid inside the joint.
Results of an animal study conducted by Ingram et al discovered that synoviocytes synthesize and secrete hyaluronan in response to cyclic movement of the joint.8 Joint immobilization reduced the concentration of hyaluronan in the synovial fluid,9 decreasing joint lubrication and synovial viscosity and increasing the coefficient of friction between articular cartilages of the synovial joints. Immobilization also decreased the activity and presence of synovial intimal cells compared with active controls, suggesting the existence of mechanosensitive homeostatic mechanisms.9
Synovial fluid exhibits non-Newtonian flow characteristics, meaning fluid viscosity either increases as the fluid is subjected to a low shear rate over time (rheopectic effect) or the fluid viscosity decreases with exposure to a high shear rate (shear-thinning effect).The viscous dissipation effect refers to heat generation from irreversible work done by fluid motion to overcome layers of shear forces in the flow. This viscous dissipation effect manifests as an increase in synovial fluid temperature.10
A case study conducted by Hor et al demonstrated this viscous dissipation effect occurring in the synovial fluid, following oscillations of an artificial hip joint — a finding quite pertinent to patients with OA who have undergone joint replacements.10 This also explains the concept of injections of shear-thinning, hyaluronan-based fluid hydrogels into the synovium of patients with OA to delay the need for arthroplasty.12
Repetitive oscillating movements that occur during walking or daily joint movement increase the joint temperature as heat is generated, both from muscle contractions and the viscous dissipation effect in the synovial fluid. Movement also stimulates the production of hyaluronan, which lubricates the joint and increases ease of motion with a lowered coefficient of friction at the articular surfaces.
These findings explain one of the cardinal symptoms reported by patients with OA: joint stiffness that is typically worse first thing in the morning or after prolonged periods of inactivity. However, they often report that this stiffness and the accompanying pain improves gradually after repeatedly moving the joint.
Flexibility and stretching exercises also help to restore the length-tension balance of the muscles surrounding joints affected by OA. Individuals with OA are prone to developing contractures. However, routine stretching and flexibility training have been found to improve joint range of motion and functional mobility, as well as reduce OA-related contractures and pain with moderate-quality evidence, according to a systematic review and meta-analysis of the literature conducted by Campbell et al.13
Targeted flexibility exercises may also benefit patients with OA prior to arthroplasty.14 Orthopedic surgeons often refer patients with OA to a physical therapist for preoperative assessment of functional impairments, customized exercise recommendations, and a preoperative physical therapy program for the purpose of optimizing surgical outcomes.
Exercise Improves Muscle Strength and Activation
Exercises that progressively strengthen muscles can have numerous benefits for individuals with OA. Arthrogenic muscle inhibition and motor weakness are neurally-mediated consequence of OA disease processes that cause pain, swelling, and inflammation, which in turn activate nociceptor and mechanoreceptor discharges that prevent full activation and contraction of muscles surrounding the affected joints. This neural inhibition can contribute to muscle weakness and atrophy15 and presents as a significant challenge to effective rehabilitation in patients with OA, even after surgery.16
In one study, Rice et al reported that individuals with OA demonstrated γ-loop dysfunction compared against those without OA.15 This finding may explain the marked quadriceps weakness and atrophy seen with arthrogenic muscle inhibition. Muscles around the joints affected by OA do not demonstrate normal motor unit recruitment secondary to dysfunctional spinal reflex pathways, such as the gamma-loop spindle system,16,17 the flexion reflex,16 and the group I nonreciprocal inhibitory pathway.16 Neuromuscular electrical stimulation, transcutaneous electrical nerve stimulation, and cryotherapy in conjunction with pain-relievers and anti-inflammatory therapies may help patients with OA overcome this barrier to muscle activation.16
Other aspects that may accelerate the progression of OA are joint instability18 and impaired neuromuscular control around the joint, as evidenced by impaired varus-valgus proprioception in individuals with medial knee OA.19 Some patients may be at greater risk of developing OA due to ligamentous laxity and proprioceptive impairment, either from previous joint injuries18 or genetic comorbidities, such as connective tissue disorders.20 Other individuals with OA may demonstrate impaired neuromuscular stabilization of the affected joint.19
Muscle strengthening can restore proprioceptive awareness and increase neuromuscular stabilization of the joint by balancing the strength of the periarticular muscles and offloading stress on the articular cartilage.18 Results of a randomized controlled trial (RCT) by Mikesky et al demonstrated that strength training for 30 months compared with range of motion exercises alone resulted in a decreased mean rate of joint space narrowing, implying that increased muscle strength delayed the progression of OA.21
In terms of exercise frequency, duration, and intensity, 3 or more exercise therapy sessions per week demonstrated increased effectiveness for addressing OA-related symptoms and impairments, compared with sessions occurring less than twice per week; although, exercising twice per week may be more acceptable for individuals who are new to exercise or who have more comorbid conditions.22 The ACSM currently recommends the following exercise prescription for individuals with hip and knee OA: 2 sessions per week with 2 to 4 sets of 8 to 12 repetitions at an intensity between 60% to 80% of the individuals 1-repetition maximum for exercises customized to address muscle strength deficits.22
Therapeutic Exercise and Manual Therapy Provide OA Pain Relief and Improve Functional Mobility
Current evidence suggests that muscle strengthening, flexibility exercises, and manual therapy effectively reduce OA-related pain and disability.23-26 If land-based exercises with full loading of the joint are too painful, water-based exercises may allow individuals with OA to stay physically active, while offloading the painful joint.27
Physical therapists prescribe home exercises so that individuals can independently maintain and progress the gains made during therapy sessions. Continuation of these exercises is critical to prevent loss of function, optimize outcomes, and prevent the return of OA symptoms among this population.27
Proprioception/Balance/Kinesiophobia
In a comparative study, Mani et al found that individuals in the earliest stages of knee OA demonstrated loss of proprioception in the hip and ankle joints.28 Lack of neuromuscular and proprioceptive control over adjacent joints can increase stress at the knee joint, potentially accelerating OA disease progression. Studies have also indicated that OA itself can contribute to reduced proprioceptive capabilities due to dysfunctional articular mechanoreceptors, particularly in severe cases of OA.29
Loss of proprioception, arthrogenic muscle inhibition, and avoidance of painful exercise fuels kinesiophobia — the fear of moving. Individuals with OA report a significant fear of falling and injury related to loss of proprioception and decreased range of motion.30 Kinesiophobia, in turn, accelerates disuse atrophy and muscle weakness by discouraging functional mobility, allowing OA to progress.
Weight Loss Through Exercise May Slow OA Progression
Decreased desire or ability to move due to OA-related pain or symptoms may result in increased sedentary lifestyles and weight gain. Weight gain increases joint compressive forces from external reaction forces due to increased load and the larger muscle contractions that are generated.31
Messier et al reported that knee joint compressive forces increase 4-fold for every pound increase in body weight.32 According to another study by Felson et al, the effect of body weight on the progression of knee OA depends on limb alignment. Moderate degrees of knee joint malalignment (genu valgus or varus) together with excess loading due to increased body weight elevated compartmental pressure in the knee joint. This elevated pressure amplified the risk for structural progression of knee OA, resulting in increased articular cartilage and meniscal degradation in compartments with decreased joint space.33
Disease-Modifying Effects of Exercise on OA
Interestingly, both overuse34,35 and disuse34,36,37 of joints contribute to the physiological degradation of the cartilage by upregulating matrix metalloproteinases in articular cartilage, resulting in tissue degradation.34 Excessive mechanical loading activates the gremlin-1-NF-κB pathway, contributing to OA pathogenesis via cartilage degeneration.35 Similarly, mechanical unloading and immobilization induce thinning of the articular cartilage by accelerating aggrecan catabolism and matrix mineralization in chrondrocytes, as well as cartilage matrix degradation and resorption via subchondral osteoclasts.36 Immobilization also alters proteoglycan synthesis.37
Located in the extracellular matrix of cartilage, proteoglycans retain water, giving cartilage the biomechanical ability to absorb high compressive loads. Proteoglycans also protect and regulate the activity of proinflammatory chemicals, growth factors, and morphogens during remodeling and repair of cartilage following tissue injury. Both OA disease processes and joint immobilization trigger proteoglycan degradation and loss of the extracellular matrix, resulting in severe changes to cartilage homeostasis.38
To combat these degenerative changes seen in OA, moderate loading of the joints promotes and maintains integrity of the articular cartilage.34 Results of an RCT conducted by Roos et al revealed that individuals at risk for knee OA who participated in moderate exercise demonstrated increased proteoglycan content in their knee cartilage, as seen on gadolinium-enhanced magnetic resonance images taken after completing supervised exercise 3 times per week for 4 months.39
Moderate loading of the joints is essential to prevent OA progression. Exercise itself can have disease-modifying effects with less likelihood of harmful side effects or unsustainable outcomes, compared with the long-term pharmacological management of symptoms.40-42
Low Impact Exercises
Both excessive joint loading and immobilization contribute to the progression of OA. Healthcare professionals who specialize in movement rehabilitation and exercise prescription, such as physical therapists, can guide individuals with OA by developing a customized therapeutic exercise program to optimize outcomes. This can simultaneously minimize pain, weight gain, and other negative effects while improving strength, range of motion, balance, and functional mobility.39
It is important to educate individuals with OA about the need to avoid exercises that may cause further harm to the joint integrity, encouraging avoidance of repetitive, high impact activities such as running and jumping.43 Walking, cycling, swimming, and water aerobics are low impact activities that reduce stress on the affected joints while also providing moderate amounts of joint loading, movement, and strengthening.4
In short, motion is lotion for osteoarthritic joints. And exercise really is medicine.
"
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