Physiatry in Motion Issue #11 ___ August 7, 2018

Updates from the AAP RFC Chair

By Allison Bean, MD, PhD

Summer is always a time of transition as a trainee in medicine. Every July we say emotional goodbyes to graduates and warmly welcome new classes. We are given more advanced roles and additional responsibilities. We begin preparation for the next phase or our careers. During this busy time, I encourage everyone to take a few moments to reflect on your growth over the past year. It can be hard to see between 24 hour calls and the seemingly infinite amounts of information we are expected to absorb, but each year we become more knowledgeable and capable, a step closer towards becoming the physiatrists of tomorrow.

The Association of Academic Physiatrists (AAP) Resident/Fellow Council (RFC) focuses on providing support to physiatrists-in-training through the AAP’s broader mission of "creating the future of academic physiatry through mentorship, leadership, and discovery” and I am proud to say that the RFC has made significant contributions to each aspect of this mission over the past year.

Mentorship – Working with the AAP Medical Student Council, the medical student mentorship program continues to grow. Through this program, medical students interested in physiatry are paired with current residents to ask questions about what life is like as a physiatry resident and get advice on how to best prepare for applying to a PM&R residency. This is particularly valuable to those students whose home institutions do not have a PM&R department. For any medical students interested in being paired with a resident mentor, or residents interested in becoming a mentor, please contact the RFC Medical Student Affairs Representative, Wyatt Kupperman, at wyatt.kupperman@sinai.org.

Leadership – The RFC is dedicated to providing a voice for trainees in physiatry, ensuring we are prepared to become the future leaders in the field. We have been working closely with the AAP Program Committee to ensure a valuable learning and training experience for PM&R trainees at Physiatry '19, to be held February 19-23, 2019 in San Juan, Puerto Rico. Trainee-focused workshops will include opportunities for hands-on workshops covering common procedures, wheelchair prescription writing, and challenging cases in ASIA classification. We also encourage all trainees to attend the highly popular fellowship roundtable and career pearls sessions where residents and fellows can get advice from experienced faculty on the next steps of their career. There will also be expanded sessions for medical students to learn how to succeed on a PM&R elective and match at their program of choice. Last but not least, there will be a RFC social event where trainees can network and relax with their peers! Further details will be provided closer to the meeting. We highly encourage all trainees to submit their research and case abstracts for Physiatry ’19 before the September 7th deadline! Information on abstract submission can be found here!


Discovery - Over the past six months, the RFC has been collaborating with AJPM&R Editor-in-Chief, Walter Frontera, MD, PhD and Associate Editor, Dinesh Kumbhare, MD, PhD to create a new section of the AJPM&R with publications authored by trainees, focusing on topics relevant to physiatry research and training. Through a national application process, Drs. Frontera and Kumbhare selected five current PM&R residents and fellows to serve as the inaugural Residents and Fellows Section (RFS) Editors. The editors are currently finalizing the author submission guidelines, and will begin soliciting article submissions soon. We hope that this will encourage medical students, residents, and fellows to learn more about research and peer-reviewed journal publication. Keep an eye out for the call for papers in the near future!

The RFC is dedicated to representing all residents and fellows. Please let us know if you have any questions or comments about what we can do to help you grow into the future leaders in physiatry by emailing us at residentfellowcouncil@gmail.com or posting on the new RFC forum.

You can also find out more information about the RFC on the AAP website and on social media!

Website: http://www.physiatry.org/page/AbouttheRFC

Facebook: AAP Residents/Fellows/Students

Instagram: @aaphysiatrists

Twitter: @AAPhysiatry_RFC

Allison Bean, MD, PhD is the 2018–2019 Chair of the AAP Residents/Fellows Council and a PGY-4 Chief Resident in the Department of Rehabilitation Medicine at the Icahn School of Medicine at Mount Sinai. Follow her on Twitter: @AlliBeanMDPhD

Developing a Career in General Physiatry: An Interview with Dr. Maria Twichell

By Marissa Pavlinich, MD

I connected with Dr. Maria Twichell, who is currently a general physiatry attending at the University of Pittsburgh Medical Center, to discuss her experiences pursuing general physiatry as a career.

What attracted you to general physiatry rather than a physiatric subspecialty?

I love the variety! Every day, I see patients with concussion, burn injury, recent polytrauma, stroke, amputation, critical illness myopathy, neuropathy, back pain, joint ailments, etc. Each case is so unique. I like having the first crack at management and procedures, but I’m also glad that I can refer the more complex patients to my specialized colleagues. Watching the daily improvement of the patients I get the privilege to treat is so rewarding.

Which factors did you find to be the most important in choosing your first general physiatry job?

I wanted a dynamic department with an excellent reputation that was growing and contributing to medical knowledge as well as the community. I envisioned working in a department that was well-integrated and respected by the surrounding health care system. I wanted a work environment that was supportive and collegial, where I could enjoy coming in every day. A degree of flexibility in order to balance my family’s schedule was also important to me.

What did you do early in your career that enabled you to define your patient population and recruit the types of patients that you were most interested in caring for?

Whenever possible, highlight your skillset. There are certain things I am not interested in doing—EMGs for example. I was able to discuss my preferences up front, then let my department chair know where I could contribute instead of doing EMGs. Efficient consults are within my skillset, but another colleague may not feel as comfortable in that role. In this way, you can further define your practice preferences.

In addition, don’t be afraid to market your skills to providers that could be referral sources. Showcase what you can do for their patients and reach out to them via the email or phone call to discuss specific cases. Close the loop. Word of good work spreads fast, so you can expect increased referrals if you provide excellent care and follow it up with feedback.

How do you maintain a balance between inpatient and outpatient medicine duties?

The secret is to be as efficient as possible so that the majority of your inpatient responsibilities and time-stamped documentation is completed prior to beginning outpatient clinic. Completing your outpatient notes during or just after clinic will reduce the amount of angst about closing your charts prior to restarting the next day. Your documentation will also be more accurate. Staying as close to caught up as possible is the key!

What do you like most about practicing as a general physiatrist?

As a general physiatrist, you get to define your own path. There is no patient population or practice environment that is out of your realm. You can choose how to evolve and grow over time.

What advice would you give to residents considering a general physiatry practice?

You absolutely are ready! It’s intimidating to think about being the most responsible provider (attending physician), but everything you have accomplished to this point has prepared you well. A strong residency program has provided you with the skills necessary to be an excellent general physiatrist. There is a learning curve, of course, but you never stop learning. Every patient you see is an opportunity to learn something, so take every day as a chance to enhance your knowledge, compassion, and skillset.

Marissa Pavlinich, MD is a PGY4 at the University of Pittsburgh Medical Center who is interested in interventional pain medicine.

Introduction to Pediatric Physiatry

By Naomi Kaplan, MBBS

As is often said, “Children aren’t tiny adults.” Pediatric physiatry has breadth and depth that few outside the field are familiar with. Pediatric physiatrists work in both inpatient and outpatient settings, providing care for children of all ages: from infants with torticollis to adolescents with cerebral palsy heading off to college. Caring for the disabled child with a patient and family-centered approach is at the heart of every pediatric rehab encounter.

Pediatric rehabilitation departments are sprinkled across the country and families often must drive many hours and miles for their child to be seen by a specialist. Outpatient departments often run clinics where children are seen by a physiatrist, multiple therapists, as well as providers from other pediatric sub-specialties (such as urology, orthopedic surgery and pulmonology). These monthly, or bimonthly, multidisciplinary clinics are particularly helpful in managing complex conditions such as cerebral palsy, spina bifida, neuromuscular conditions and limb deficiencies. “General” clinic appointments provide interim follow-up and allow specific problems to be addressed.

Procedures are an established part of pediatric physiatry, whether they be toxin injections, baclofen pump management or EMGs. Children present a unique challenge, not always being able to tolerate needle sticks and sometimes requiring oral or IV sedation. Toxin injection is being done under EMG, e-stim, and increasingly ultrasound guidance.

Children are still developing in all aspects of their being, from a cognitive, emotional, and physiological standpoint. Static insult or injury can have chronic effects, as the child continues to develop. Knowledge of normal pediatric developmental milestones is integral to the practice of pediatric physiatry.

There are many allied health professionals, not often seen in the adult realm, who provide enrichment and therapy for the pediatric patient, allowing the child to stay engaged in treatment, stimulated by their environment, and emotionally and psychologically grounded during chronic medical treatment and rehabilitation. These include, but are not limited to Child Life specialists, licensed massage therapists, music therapists and child psychology. Incentivization, through use of sticker charts, hospital “money,” and rewards, is a challenging but fun aspect of pediatric rehabilitation used to maximize participation and help achieve specific functional goals.

The importance of advocacy for the pediatric physiatry patient cannot be overstated. These patients are vulnerable with complex needs. Guardians have a responsibility to bring patients to their appointments. The team should help to facilitate clinic attendance by sending timely reminders and assisting with transportation barriers. Social workers are an important part of the pediatric rehab team, but the safeguarding of children is everyone’s responsibility. Cases of non-accidental trauma or abuse require input from all angles, to ensure safe discharge planning for the patient and appropriate documentation.

Pediatric physiatry is a field ripe with research opportunities, from bench work to clinical trials. Qualitative and quantitative research can be initiated, as well as quality improvement studies.

Pediatric rehabilitation is an expansive and rewarding sub-specialty with an opportunity for great career satisfaction. Maria Montessori once said, “Play is the work of children,” and pediatric physiatry is the path to play, function and quality of life.

Naomi Kaplan, MBBS, is a PGY-4 resident in PM&R at Zucker SOM at Hofstra/Northwell with an interest in pediatric rehabilitation.

The Role of PM&R in One Life

By Lisa Wiesenberger

My sister has a specific way that she walks. Her gait is unusual and one that I can immediately recognize. There is a sort of shuffling and dragging of the right foot that seems to slightly lag behind as she steps forward with her left foot. To a stranger’s eyes, it may appear that she has trouble walking, but in my eyes, I see the victory of rehabilitation medicine that made walking an improbable possibility.

My older sister, Selina, is a twenty-five year old with Down Syndrome who has an array of severe physical and developmental complications. She underwent two spinal surgeries for severe atlantoaxial instability and has spent most of her life wearing ankle foot orthoses (AFOs) to steadily improve her balance and gait over time. I grew up carefully watching how her care team, particularly her pediatric physiatrist, cared for Selina and nurtured her to become a strong, independent individual, both physically and mentally. Before my eyes, the physiatrists and physical therapists used their expertise and the latest technology in the field of physical medicine and rehabilitation to transform Selina’s musculoskeletal strength and coordination. Through the years I watched my sister progress from a wheelchair, to a walker, to her feet (still in AFO’s), and to the front stage to continue her love of dancing.

Selina 2001

As her sister, I witnessed the power of healing that physical medicine and rehabilitation can provide. This has instilled in me a deep appreciation for the role of PM&R in healthcare. PM&R goes beyond medicine and improves function, long term outcomes and quality of life. These are a few reasons why I believe PM&R is unique and why many of us are drawn to the field. It is a commitment to bettering the lives of patients in the way that it has for Selina.

Selina 2017

Lisa Wiesenberger is an MS3 at the Central Michigan University College of Medicine who is interested in PM&R.

The Role of Nutrition in Osteoarthritis

By Caroline Schepker, DO

Osteoarthritis (OA) is the fastest growing form of disability worldwide (1), and treatment options for symptomatic OA are fairly limited and often only provide temporary relief. Furthermore, OA has classically been considered a non-inflammatory arthritis while only rheumatologic arthritides were considered inflammatory in nature. However, recent research suggests an underlying low-grade inflammatory component to OA that may be rooted in chronic systemic inflammation and the metabolic syndrome (2,3,4). Furthermore, synovitis has recently been identified as a hallmark feature of OA. Other critical features likely involve subchondral bone as a source of inflammatory mediators, as well as the release of matrix metalloproteinases by cartilage in response to both systemic and localized cytokines and prostaglandins (5). Increased adiposity is associated with adipokine release and activation of pro-inflammatory interleukins. Hyperglycemia and high LDL cholesterol are also independently associated with systemic inflammation. These systemic metabolic derangements could possibly be playing a role in triggering pain attacks in patients with non-post-traumatic osteoarthritis.

The role of addressing systemic inflammation through lifestyle, particularly dietary modifications, dates back several thousand years to the advent of Ayurvedic and Traditional Chinese Medicine dietary practices, which have historically sought to address arthritis by eliminating foods that produce “heat” in the body and emphasize “cooling” foods. More recent research examining the effects of diet on the most inflammatory form of arthritis—rheumatoid arthritis (RA)—suggests that these age-old traditions might have had something right. There is an abundance of literature examining dietary interventions in rheumatologic diseases, given the high concordance of these conditions with gastrointestinal diseases such as IBD. Fraser et al. studied a group of RA patients who were advised to engage in “subtotal fasting”—they were allowed to consume a limited amount of vitamin and mineral supplementation, carbohydrate, and energy in the form of vegetable juice for one week. As compared with controls, this group was found to have decreased CD4+ lymphocyte activation and numbers—a process indicative of progression of RA. Their theory was that transient immunosuppression was able to suppress the pro-inflammatory process underlying RA (6). Michalsen et al. also showed clinical improvement in RA patients who underwent fasting protocols (7). Kjeldsen-Kragh et al. asked RA patients to fast for 7-10 days with partial nutrient intake of vegetable broth, herbal teas, parsley, garlic, potatoes, and juice extracts from carrots, beets, and celery. This period was followed by either one year of a 100% plant-based (vegan) diet or an omnivorous diet. The participants who followed the fast with a vegan diet demonstrated statistically significant clinical decreases in swollen and tender joints and pain, as well as blood markers of inflammation (ESR and CRP) (8).

Thomas et al. performed a literature review of the relevance of dietary interventions to OA management in 2018. This group found six modifiable nutritional factors that may be implicated in OA: adiposity/obesity, metabolic syndrome, type 2 diabetes, consumption of long-chain n-3 fatty acids, blood cholesterol levels, and vitamin K intake (9).

Adiposity and Obesity: Obesity increases axial load compression on weight bearing joints; over time, overweight and obese individuals are increasingly more likely to electively have a knee replaced than their normal-weight counterparts (10). Interestingly, higher BMI is also associated with higher risk for OA in non-weight-bearing joints as well—particularly the hand—which suggests a non-mechanical and perhaps inflammatory or biochemical etiology (11). One theory underlying the inflammatory role of fat tissue lies in adipokines—proteins secreted by adipocytes that trigger a cascade of pro-inflammatory cytokines. Leptin is a specific adipokine that is elevated in the postprandial state and is often chronically elevated in obesity. High blood levels of leptin are also independently associated with inflammation and cartilage degradation (12, 13).

Metabolic Syndrome: The metabolic syndrome is defined as the coexistence of central obesity, insulin resistance, dyslipidemia, and hypertension. The Research on Osteoarthritis/Osteoporosis Against Disability cohort (n=1384) showed increased radiographic incidence and progression of knee OA with accumulation of components of the metabolic syndrome; this was similarly observed in the Melbourne Collaborative Cohort Study (14, 15). Possible mechanisms underlying this correlation include increased systemic inflammation, higher axial compression/weight bearing secondary to increased BMI, and impaired blood flow to microvasculature in the setting of dyslipidemia and atherosclerotic disease, which may ultimately prolong and impair healing and repair from the daily wear-and-tear on bones and soft tissues of the musculoskeletal system.

Type 2 Diabetes: Impaired glucose tolerance and prolonged, chronically elevated blood sugar results in accumulation of AGEs, or advanced-glycation end products—proteins and lipids that become glycated when exposed to sugars. AGEs are believed to play a role in the pathogenesis of many degenerative diseases including atherosclerosis, chronic kidney disease, and neurodegenerative diseases. AGEs induce a pro-coagulant state, vasoconstriction, pro-inflammatory cascades, free radical formation, and lipogenesis. A German cohort study found type 2 diabetes to be an independent risk factor for severe OA, as well as a predictor for knee and/or hip replacement (16). A subsequent French study assessed patients with knee OA over 3 years; type 2 diabetes was again a statistically significant predictor of reduction of joint space width in men (17).

Dietary lipids: Interestingly, dietary lipids can make their way into the matrix and chondrocytes of articular cartilage and act as a source of inflammation—a study by Plumb et al. found high levels of pro-omega-6 fatty acids, precursors to pro-inflammatory eicosanoids, in cores of cancellous bone taken from the femoral heads of patients undergoing orthopedic surgery to address OA (18). Furthermore, in individuals with knee OA, a positive correlation has been identified between serum levels of the omega-6 polyunsaturated acid arachidonic acid and synovitis; conversely, an inverse relationship has been identified between serum levels of omega-3 docosahexaenoic acid (DHA) and patellofemoral cartilage loss as measured by MRI (19). Finally, a larger prospective study of OA patients found that higher intakes of both total fat and saturated fat were associated with increased radiographic evidence of knee joint space loss (20). The Western diet typically boasts a high ratio of omega-6 to omega-3 fatty acids, which may predispose individuals to inflammation. Arachidonic acid, a metabolite of omega-6 fatty acids, is pro-inflammatory and typically sourced from animal fats such as meats, dairy, and eggs, as well as some vegetable oils—namely safflower and sunflower oil. EPA and DHA, anti-inflammatory metabolites of omega-3 fatty acids, are predominant in walnuts, flaxseeds, and algae- or fish-based oil supplements.

Cholesterol: Dyslipidemia has long been identified as an independent risk factor for OA—backed by several epidemiologic studies (21, 22, 23). An Australian cohort of healthy middle-aged women found that, for every 1 mmol/L increase in total serum cholesterol, the adjusted odds of developing a bone marrow lesion were 1.84 (24). Statin use seems to ameliorate some of the symptoms of OA—a 10-year longitudinal study in a cohort of 16,609 participants found that increasing statin dose in dyslipidemic patients was associated with decreased clinical features of OA (25). Statin use was also found to be associated with improved imaging findings—resulting in over 50% reduction in radiographic progression of knee OA (26). It is possible that this effect could be mediated not only by the LDL-reducing effects of statins, but also by their anti-inflammatory effects; statins have been shown to reduce expression of inflammatory cytokines and exert chondroprotective effects—with atorvastatin in particular inhibiting interleukin 1B and matrix metalloproteinase 13 in vitro (27). The mechanisms underlying the interplay between serum cholesterol and OA are unclear—but cholesterol, like fatty acids, has also been found to accumulate in the articular cartilage of individuals with OA, and high LDL in particular may play a direct role in triggering synovitis and subsequent osteophyte formation (28). Statins may not be necessary; dietary and exercise interventions alone can have dramatic affects on lipid profile. Strategies include restricting saturated fat to 11% or less of total energy, generous consumption of soluble fiber, moderate consumption of soy protein (25g/daily), and a dietary foundation in plant sterols and stanols—found in virtually all whole plant-based foods. In fact, there appears to be a dose-effect relationship between plant stanols and LDL cholesterol, with 9-10g of daily stanols lowering LDL cholesterol by 18% (29).

Vitamin K: Vitamin K is involved in bone and cartilage mineralization, and is largely obtained in the diet from green leafy vegetables (vitamin K1) and bacteria (vitamin K2). Suboptimal vitamin K intake may cause decreased carboxylation of vitamin-K dependent proteins, which induce anabolic processes in bone and cartilage (30). In several longitudinal studies, individuals who were deficient in vitamin K were more likely to have articular cartilage and meniscal damage in the knees (31, 32). Only one randomized, controlled trial examining the effect of vitamin K supplementation on OA exists—and although it failed to find a beneficial effect of supplementation on progression of OA, only a small percent of the cohort was truly vitamin K deficient at baseline. Within that small group, those who achieved therapeutic blood levels demonstrated 47% less joint space narrowing at follow-up (p = 0.02)(33).

Conclusions: Osteoarthritis, which was once believed to be a pure reflection of years of mechanical wear-and-tear on joints, is in reality a complex degenerative disease that likely has roots in the underlying health of the individual. OA risk factors may be even more heavily modifiable than many clinicians consider or address with their patients. Chronic, low grade systemic inflammation from diet and adiposity; suboptimal blood flow secondary to increased viscosity from hyperglycemia and hypercholesterolemia; subtle underlying nutritional deficiencies that hamper optimization of growth and repair mechanisms; research has only begun to scratch the surface of the many factors at play. However, when taken as a whole, many of these modifiable risk factors can be addressed in the same way: by prioritizing a whole foods and plant-rich diet—one that is relatively low in energy density to support normalization of weight, high in fiber and plant sterols/stanols to promote healthy blood lipid levels, and high in leafy greens and omega 3 fatty acids to support optimal micro- and macronutrient intake. In 2015, a six-week, prospective, randomized study of 37 patients aged 19-70 with symptomatic OA found statistically significant improvements in self-reported energy, physical functioning, joint mobility, and pain in the group randomized to a whole-foods plant-based diet as compared with participants who ate their usual diets (34). As we progress in our understanding of the complex underlying biochemical and endocrinological underpinnings of this disease, we just may come to appreciate the efficacy of the simplest of approaches to symptom management and the slowing of disease progression.


(1) Conaghan PG, Porcheret M, Kingsbury SR et al. Impact and therapy of osteoarthritis: the Arthritis Care OA Nation 2012 survey. Clin Rheumatol 2015; 3:1581.

(2) Sturmer T, Brenner H, Koenig W, Gunther KP. Severity and extent of osteoarthritis and low grade systemic inflammation as assessed by high sensitivity C reactive protein. Annals of the Rheumatic Diseases 2004; 63:200-205.

(3) Zhuo Q, Yang W, Chen J, Wang Y. Metabolic syndrome meets osteoarthritis. Nature Reviews: Rheumatology 2012; 8:729-737.

(4) Engstrom G, Gerhardsson de Verdier M, Rollof J et al. C-reactive protein, metabolic syndrome and incidence of severe hip and knee osteoarthritis: a population-based cohort study. Osteoarthritis and Cartilage 2009; 17:168-173.

(5) Berenbaum F. Osteoarthritis as an inflammatory disease. Osteoarthritis and Cartilage 2013; 21:16-21.

(6) Fraser D, Thoen J, Reseland J et al. Decreased CD4+ lymphocyte activation and increased interleukin-4 production in peripheral blood of rheumatoid arthritis patients after acute starvation. Clin Rheumatol 1999; 18:394-401.

(7) Michalsen A, Riegert M, Ludtke R et al. Mediterranean diet or extended fasting’s influence on changing the intestinal microflora, immunoglobulin A secretion and clinical outcome in patients with rheumatoid arthritis and fibromyalgia: an observational study. BMC Complement Altern Med 2005; 5:22.

(8) Kjeldsen-Kragh J, Borchgrevink C, Laerum E et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet 1991; 338:899-902.

(9) Thomas S, Browne H, Mobasheri A et al. What is the evidence for a role for diet and nutrition in osteoarthritis? Rheumatology 2018; 57:iv61-iv74.

(10) Leyland KM, Judge A, Javaid MK et al. Obesity and the relative risk of knee replacement surgery in patients with knee osteoarthritis: a prospective cohort study. Arthritis Rheumatol 2016; 68:817-25.

(11) Yusuf E, Nelissen RG, Ioan-Facsinay A et al. Association between weight or body mass index and hand osteoarthritis: a systematic review. Ann Rheum Dis 2010; 69:761-765.

(12) Hui W, Litherland GJ, Elias MS et al. Leptin produced by joint white adipose tissue induces cartilage degradation via upregulation and activation of matrix metalloproteinases. Ann Rheum Dis 2012; 71: 455-462.

(13) Scotece M, Mobasheri A. Leptin in osteoarthritis: focus on articular cartilage and chondrocytes. Life Sci 2015; 140: 75-78.

(14) Yoshimura N, Muraki S, Oka H et al. Accumulation of metabolic risk factors such as overweight, hypertension, dyslipidaemia, and impaired glucose tolerance raises the risk of recurrence and progression of knee osteoarthritis: a 3-year follow-up of the ROAD study. Osteoarthritis Cartilage 2012; 20:1217-1226.

(15) Monira Hussain S, Wang Y, Cicuttini FM et al. Incidence of total knee and hip replacement for osteoarthritis in relation to the metabolic syndrome and its components: a prospective cohort study. Semin Arthritis Rheum 2014; 43: 429-436.

(16) Schett G, Kleyer A, Perricone C et al. Diabetes is an independent predictor for severe osteoarthritis: results from a longitudinal cohort study. Diabetes Care 2013; 36: 403-409.

(17) Eymard F, Parsons C, Edwards MH et al. Diabetes is a risk factor for knee osteoarthritis progression. Osteoarthritis Cartilage 2015; 23: 851-859.

(18) Plumb MS, Aspden RM. High levels of fat and n-6 fatty acids in cancellous bone in osteoarthritis. Lipids Health Dis 2004; 3:12.

(19) Baker KR, Matthan NR, Lichtenstein AH et al. Association of plasma n-6 and n-3 polyunsaturated fatty acids with synovitis of the knee: the MOST study. Osteoarthritis Cartilage 2012; 20: 382-387.

(20) Lu B, Driban J, Xu C et al. Dietary fat and radiographic progression of knee osteoarthritis: data from the Osteoarthritis Initiative. Arthritis Care Res 2017; 69: 368-375.

(21) Hart DJ, Doyle DV, Spector TD. Association between metabolic factors and knee osteoarthritis in women: the Chingford Study. J Rheumatol 1995; 22: 1118-1123.

(22) Sturmer T, Sun Y, Sauerland S et al. Serum cholesterol and osteoarthritis: The baseline examination of the Ulm Osteoarthritis Study. J Rheumatol 1998; 25: 1827-1832.

(23) Addimanda O, Mancarella L, Dolzani P et al. Clinical associations in patients with hand osteoarthritis. Scand J Rheumatol 2012; 41: 310-313.

(24) Davies-Tuck M, Hanna F, Davis SR et al. Total cholesterol and triglycerides are associated with the development of new bone marrow lesions in asymptomatic middle-aged women – a prospective cohort study. Arthritis Res Ther 2009; 11: R181.

(25) Kadam UT, Blagojevic M, Belcher J. Statin use and clinical osteoarthritis in the general population: a longitudinal study. J Gen Intern Med 2013; 28: 943-949.

(26) Clockaerts S, Van Osch GJ, Bastiaansen-Jenniskens YM et al. Statin use is associated with reduced incidence and progression of knee osteoarthritis in the Rotterdam study. Ann Rheum Dis 2012; 71: 642-647.

(27) Simopolou T, Malizos KN, Poultsides L, et al. Protective effect of atorvastatin in cultured osteoarthritic chondrocytes. J Orthop Res 2010; 28: 110-115.

(28) Cillero-Pastor B, Eijkel G, Kiss A et al. Time-of-flight secondary ion mass spectrometry-based molecular distribution distinguishing healthy and osteoarthritic human cartilage. Anal Chem 2012; 84: 8909-8916.

(29) Laitinen K, Gylling H. Dose-dependent LDL-cholesterol lowering effect by plant stanol ester consumption: clinical evidence. Lipids Health Dis 2012; 11: 140.

(30) Beckner KL. Vitamin K dependent carboxylation. Vitam Horm 2008; 78: 131-156.

(31) Shea MK, Kritchevsky SB, Hsu FC et al. The association between vitamin K status and knee osteoarthritis features in older adults: the Health, Aging, and Body Composition Study. Osteoarthritis Cartilage 2015; 23: 370-378.

(32) Misra D, Booth SL, Tolstykh I et al. Vitamin K deficiency is associated with incident knee osteoarthritis. Am J Med 2013; 126: 243-248.

(33) Neogi T, Fleson DT, Sarno R et al. Vitamin K and hand osteoarthritis: results from a randomized controlled trial. Ann Rheum Dis 2008; 67: 1570-1573.

(34) Clinton C, O’Brien S, Law J et al. Whole-foods, plant-based diet alleviates the symptoms of osteoarthritis. Arthritis 2015; 2015: 708152.

Caroline Schepker, DO is a PGY3 in PM&R at NYP-Columbia/Cornell who is interested in musculoskeletal and integrative medicine.


In our 9th issue, we mistakenly did not include the introduction of one new member of the 2018-2019 Resident Fellow Council. We apologize for the omission and would like to introduce her now.

Marissa Pavlinich is the 2018-2019 RFC AAMC representative.

She is a PGY4 at the University of Pittsburgh Medical Center.

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