Patients and physicians share the common goal of avoiding knee replacement—when possible. As our Knee Restoration Center strives to offer the latest SCIENCE-BASED alternatives (no voodoo, crystals or “stem cell cure” hype at our center) to full knee replacement, many patients seek our guidance.
Patients continue searching for other options after being told they need total knee replacement. The vast majority over the age of 60, when told by a knee specialist that they need a replacement, in fact, need a knee replacement. While there are options/alternatives to “delay” knee replacement, these treatments are palliative and eventually knee replacement is performed.
During this search for alternatives, patients inevitably discover Cartilage Restoration. Unfortunately, it is typically too late in the disease process and cartilage restoration does not apply to them. I'm sorry to say that at this point in time cartilage restoration works best for focal defects, not end-stage loss of cartilage. Think of current restoration as “filling pot-holes" in a road and arthritis is damage to the entire road surface.
Fortunately, for future generations, scientists continue to work on biologic treatments for arthritis and we are witnessing a renewed interest in ways to modify the course of arthritis. The Knee Restoration Center is participating in a variety of knee injection trials that are directed primarily at symptomatic relief, yet with a close watch for disease modification or a type of DMOAD—Disease Modifying OsteoArthritis Drug. (You are probably aware of the success of biologic injections in the dramatic treatment of rheumatoid arthritis, psoriatic arthritis and others).
We were fortunate to be invited to participate in the two scholarly papers below with lead authors Dr. Wei Seong Toh and Dr. Mats Brittberg. While these publications are directed at scientists and clinicians, everyone can glean some information on the current “state of the art”.
Wei Seong Toh, Mats Brittberg, Jack Farr, Casper Bindzus Foldager, Andreas H Gomoll, James Hoi Po Hui, James B Richardson, Sally Roberts, Myron Spector
Abstract—It is well accepted that age is an important contributing factor to poor cartilage repair following injury, and to the development of osteoarthritis. Cellular senescence, the loss of the ability of cells to divide has been noted as the major factor contributing to age related changes in cartilage homeostasis, function, and response to injury. The underlying mechanisms of cellular senescence, while not fully understood, have been associated with telomere erosion, DNA damage, oxidative stress, and inflammation. In this review, we discuss the causes and consequences of cellular senescence, and the associated biological challenges in cartilage repair. In addition, we present novel strategies for modulation of cellular senescence that may help to improve cartilage regeneration in an aging population.
Mats Brittberg, Andreas H Gomoll, José A Conseco, Jack Farr, Martin Lind, James Hui
Background and purpose—Cartilage damage can develop due to trauma, resulting in focal chondral or osteochondral defects, or as more diffuse loss of cartilage in a generalized organ disease such as osteoarthritis. A loss of cartilage function and quality is also seen with increasing age. There is a spectrum of diseases ranging from focal cartilage defects with healthy surrounding cartilage to focal lesions in degenerative cartilage, to multiple and diffuse lesions in osteoarthritic cartilage. At the recent Aarhus Regenerative Orthopaedics Symposium (AROS) 2015, regenerative challenges in an ageing population were discussed by clinicians and basic scientists. A group of clinicians was given the task of discussing the role of tissue engineering in the treatment of degenerative cartilage lesions in ageing patients. We present the outcomes of our discussions on current treatment options for such lesions, with particular emphasis on different biological repair techniques and their supporting level of evidence.
Results and interpretation—Based on the studies on treatment of degenerative lesions and early OA, there is low-level evidence to suggest that cartilage repair is a possible treatment for such lesions, but there are conflicting results regarding the effect of advanced age on outcome. We concluded that further improvements are needed for direct repair of focal, purely traumatic defects before we can routinely use such repair techniques for the more challenging degenerative lesions. Furthermore, we need to identify trigger mechanisms that start generalized loss of cartilage matrix, and induce subchondral bone changes and concomitant synovial pathology, to maximize our treatment methods for biological repair in degenerative ageing joints.