Announcements & News

What causes the lasting insult in knee OA?

Dec 6, 2014

Interview originally appeared on December 5, 2014 | ACR 2014, Arthritis, Osteoarthritis, Rheumatologic Pain

 

Watch the video here

 

By Tuhina Neogi MD

Rheumatology Network

For some patients with knee osteoarthritis, pain signals are centralized and become more intense, rather than waning with time. Is this caused by continuing injury to the damaged knee, or is inflammation more prominent?

In this video, researcher Tuhina Neogi of Boston University School of Medicine describes research presented at the 2014 annual meeting of the American College of Rheumatology that addressed this question by assessing specific signs of inflammation (synovitis and effusion on MRI) and noninflammatory tissue injury (bone marrow lesions) with relation to the development of central sensitization of pain.

An Associate Professor at Boston University School of Medicine, Dr. Neogi studies the epidemiology of rheumatic disease.

The questions:

You've been looking at the causes of sensitization of knee osteoarthritis pain. How do you define sensitization?

Can you tell us about the study that you presented at the ACR?

We've heard a lot lately about the fact that rheumatologists are able to address inflammation but they're not so able to address pain. Do you think your findings have any practical implications with regard to what rheumatologists are or are not able to do?

If your listeners want to look for the next paper that carries this research forward, what might its title be? What should they be looking for?

Key quotes:

We and others have demonstrated that sensitization is associated with increased pain severity ... and change in pain over time. But what we didn't know is what causes sensitization in knee OA.

Inflammation likely contributes to sensitization in knee osteoarthritis, whereas bone marrow lesions do not appear to do so. Therefore, bone marrow lesions likely contribute to pain through other mechanisms.

We need to do some more studies to see if intervening early on these parameters of inflammation has an effect.

I think overall the take-home message for clinicians is that pain is a multifactorial symptom and we need to move more towards mechanism-based pain management that's not a one-size-fits-all for everyone. ... We cannot just say "This is the first step. This is the second step." It has to become more personalized.

References:

Neogi T, Nevitt MC, Scholz J, et al. Effect of Synovitis, Effusion and Bone Marrow Lesions on Development of Sensitization in Knee OA: The Multicenter Osteoarthritis Study ACR Abstract #2783, 2014 66:S1306. Abstract Supplement, 2014 ACR/ARHP Annual Meeting

Researchers on the Path to a Cure – Spotlight on Dr. Tuhina Neogi

Arthritis Foundation News Blog - April 13, 2017

Dr-Tuhina-Neogi

 

 

 

 

 

 

 

 

If you have osteoporosis you’ve probably heard of, and may have been treated with, a class of drugs that are used to prevent and treat bone loss: bisphosphonates. Dr. Tuhina Neogi and her research team are using new methods to look at how the long-term effects of using these drugs may be related to the progression of knee osteoarthritis (OA).

Dr. Neogi’s 2-year Arthritis Foundation-funded project, “Bisphosphonate Effects in Knee Osteoarthritis,” is looking at the relationship of bisphosphonate treatment and the structural changes in the knee associated with OA progression. To do this, Dr. Neogi and her team are looking at how knee joint space width, three-dimensional (3D) bone shape, and bone marrow lesions change in OA patients over time.
Dr. Neogi is interested in this research for several reasons. First, the long-term effects of bisphosphonates on knee OA is controversial due to conflicting study results and concerns about changing bone properties over time. “Bisphosphonates are used to maintain and improve bone density by improving or rebuilding (remodeling) bone in patients with osteoporosis. It helps to reduce the risk of fractures. However, remodeling bone in patients with OA may not be the same as remodeling bone in patients with osteoporosis. Changing the bones by making them stiffer may not be good for OA. On the other hand, bisphosphonates may have beneficial effects on chondrocytes (cells in the cartilage). Thus, the benefits versus the risks are not clear.”

Dr. Neogi is also interested in looking at the data in new ways to reduce the confusion found in earlier studies with conflicting or inconclusive results. Earlier studies used only x-rays to evaluate structural changes in OA. She and her team are also using magnetic resonance imaging (MRI), focusing on bone marrow lesions that can cause pain in OA, and 3-D bone shape, which can provide a more global assessment of what is going on in the joint. “Structural changes associated with OA are traditionally assessed as joint-space width on x-rays, which lack sensitivity to change. It takes a long time for joint width changes to be detected by x-rays. MRI can provide insights into how OA is changing over much shorter periods of time, and is therefore likely a better way to assess a drug’s effects on OA.”

The team is also using data from a large United Kingdom (UK) medical database to determine if taking bisphosphates can slow the progression of knee OA and make a difference in if, or when, a knee replacement may be needed. “About 97% of knee replacements are performed because of OA and is therefore a good indicator of people who have progressed to “end-stage” knee OA,” Dr. Neogi explained. Dr. Neogi and her team began this project by analyzing the data from a UK database that included information from about 13 million patients. She explained it was important to use the UK data because patients there have universal healthcare, so no one would be excluded because they could not afford or have access to medical treatment. The team chose two sets of patient groups to compare. One group included newly diagnosed OA patients who were new users of bisphosphonates. The second group included newly diagnosed OA patients who were similar to the first set (like age, sex, weight, etc.), except they were not users of bisphosphonates. After comparing the long-term data, the team found that significantly fewer patients in the bisphosphonate treatment group went on to have knee replacement surgery than the non-users.

The team is now analyzing the data from the MRI studies using data from a nationwide research study sponsored by the National Institutes of Health that is looking at knee osteoarthritis. While the analyses are not finished, they are seeing results that are similar to the UK database results. Subjects who were taking bisphosphonate treatment had less severe structural progression.

The different approaches to looking at OA outcomes are showing results pointing in the same direction. While bisphosphonate treatment may not work for everyone and additional work needs to be done on these projects, Dr. Neogi feels that her team’s research results may support some promising long-term effects of bisphosphonates and this drug class could potentially be a therapeutic option for millions of Americans with knee OA.

Dr. Neogi is a Professor of Medicine at Boston University School of Medicine and a Professor of Epidemiology at the Boston University School of Public Health.

David Felson awarded Carol Nachman Prize for Rheumatology

May 12, 2017

The 201David Felson7 Carol Nachman Prize for Rheumatology was awarded to David T. Felson, MD, MPH, Professor of Medicine and Epidemiology at BUSM and BUSPH.

David T. Felson (SPH’84), Professor of Epidemiology at the School of Public Health and of Medicine at the School of Medicine, has been awarded the 2017 Carol Nachman Prize for Rheumatology.

The prize is the most prestigious international award for research in rheumatology. Felson received the award on May 12 in Wiesbaden, Germany.

Dr. Felson’s research interests include understanding how to prevent and treat osteoarthritis (OA)—also known as degenerative joint disease, or “wear and tear” arthritis. He is studying whether treatments for rheumatic diseases are effective and, particularly in osteoarthritis, identifying risk factors for disease, testing treatments, and characterizing MRI features of normal knees and knees with pain. He also studies outcome measurement (tests that objectively determine a patients’ baseline function at the beginning of treatment) in rheumatic disease, and has focused in this work on rheumatoid arthritis trials.

Felson led a series of major studies to identify prevalence, impact, and risk factors for knee OA. In the Framingham Osteoarthritis Study, his group first documented that obesity increased the risk of OA and that weight loss could lessen that risk. The first to introduce magnetic resonance imaging in large-scale studies, his group discovered that meniscal tears and other structural pathology were present in most middle-aged and older persons regardless of knee pain. He inaugurated the study of structural correlates of joint pain, identifying for the first time that in OA, synovitis and bone marrow lesions cause pain; these structural findings have now emerged as targets of treatment. Recent work from his group suggests that chronic alterations in the nervous system that enhance pain sensitivity affect most patients with OA pain.

Working with the FDA and rheumatology organizations, he also led the effort to standardize clinical trial outcome measurement in rheumatoid arthritis, creating the first core set of outcomes and coming up with the American College of Rheumatology definition of improvement (ACR20). This outcome standardization made it possible for the first time to gauge the relative efficacy of new drugs such as TNF inhibitors.

The recipient of numerous awards, Felson was the first non-basic scientist recipient of the Kunkel Young Investigator Award from the American College of Rheumatology, and from this same organization, he received its inaugural Clinical Research Award.

Felson graduated from Harvard College and received his MD from Johns Hopkins University. After a residency in internal medicine at Case Western Reserve, he trained in rheumatology at Boston University and received his MPH in epidemiology from SPH. He joined the BU faculty in 1984, became a professor in 1994, and was appointed chair of clinical epidemiology in 2001.  He is Director of Training and Education for the BU Clinical Translational Science Institute and Director of Clinical Epidemiology at Boston Medical Center.

2017 OARSI World Congress on Osteoarthritis – Las Vegas, NV

4/27/ - 4/30/2017

Members of the unit participated with invited lectures, oral presentations, and posters.

David Felson – Invited Lecture: Metabolic OA: Does it exist?

Tuhina Neogi – Invited Lecture: Current perspectives on pain in OA

Tuhina Neogi – Invited Lecture: Effect of bisphosphonate use on trajectories of MRI-based three-dimensional bone shape of the knee over four years

Devyani Misra – Oral Presentation #822: Obesity-related systemic inflammation and knee synovitis

Kathy Bacon – Poster #642: The non-linear relationship of quadriceps strength to functional limitations in people with knee OA: The MOST Study

Reza Jafarzadeh – Poster #528: Assessing mediating effect of bone marrow lesions and synovitis following extreme weight loss on knee pain reduction

Deepak Kumar – Poster #149: Degeneration of patellofemoral and tibiofemoral compartments following ACL reconstruction and associated gait mechanics: A longitudinal 2-year study

Deepak Kumar – Poster #185: Knee loading is lower during mindful walking compared to regular walking: A preliminary study

Deepak Kumar – Poster #266: Effects of weight loss on patellofemoral loading in overweight and obese adults with patellofemoral OA: Secondary analysis from the IDEA randomized trial

Deepak Kumar – Poster #594: Vastus medialis intramuscular fat is associated with increase in MRI degeneration of the knee over 3 years

Jing-Sheng Li – Poster #468: Racial differences in MRI-based 3D bone shape of the femur vs the tibia at the knee: Data from the Osteoarthritis Initiative

Erin Macri – Poster #285: Defining abnormal cut-points for patellofemoral alignment and trochlear morphology and their relation to patellofemoral OA: The Framingham OA Study

Tuhina Neogi – Poster #30: Relation of pain sensitization to development of constant, persistent pain in knee OA: The MOST Study

Shanshan Sheehy – Poster #301: Can adipokines elucidate the sex disparity in osteoarthritis?