It is generally accepted that arthritis of the knee affects the entire joint including menisci, cartilage and synovia. While various studies suggest (partial) meniscectomy being the major trigger for subsequent osteoarthritis, some opinion leaders consider an initial cartilage defect being the reason for further joint degeneration and subsequent meniscus pathologies. What is your opinion regarding the relationship between cartilage injury/defect and meniscus injury and subsequent osteoarthritis?
Great question that I think many of us are trying to answer. I do agree that OA starts after a macrotraumatic knee injury, my thoughts are that it could be both. Interactive destructive changes in biomechanics and biochemistry could propagate one another after either incidence. The issue that still remains is what about the OA knee with no history of macrotraumatic injury at all? I agree with colleagues that OA may have different phenotypes possibly based on where the degeneration was initiated which could have major therapeutic intervention implications.
Great question - I am looking forward to others thoughts on this.
Thank you for an interesting question. I agree that this is a great question, a hot topic in translational research. From animal models we know that a joint trauma triggers osteoathritis and I have read once that approximately 50% of the rats will develop OA within a few weeks after experimal meniscal tear. But,applying this into human biology and pain physiology would be exiting. I hope long term follow up studies in large populations may generate good clinical hypotheses.
The question posed seems very interesting. In my humble opinion limited cartilage lesions can contribute to the presentation of a degenerative meniscopathy, but also the patient's age, physical activity, axis of limb , weight and repeted small trauma should be considered in the etiology of osteoarthritis of the knee. In my opinion the factors favoring osteoarthritis are fundamentally : overweight, genu varus or valgus, mechanical overload and degenerative meniscal pathology
I assume you mean osteoarthritis (OA). As above elaborated on, the initial insult seems likely to be micro or macro trauma to the cartilage or overall joint structures, with an increase first in the cartilage water content, leading later to microfibrillations, etc. The hypothesis of trauma preceding and/or leading to this disease has been documented experimentally in dogs, where a ligament is first severed, leading to post traumatic OA changes over time in that joint affected (old studies).
It would be nice if that would be the case. I am not aware of any data that prophylactic glucosamine intake would prevent the development of OA later. I just don't know. There are studies that suggest that glucosamine/chondroitin sulfate intake can delay the progression of OA; however, these studies are controversial and not everyone agrees that this is the case,
Dear Phillip
This article may be useful for you
Arthritis Care Res (Hoboken). 2013 Dec;65(12):1942-50.
Association of metabolic risk factors with cartilage degradation assessed by T2 relaxation time at the knee: data from the osteoarthritis initiative.
Jungmann PM, Kraus MS, Alizai H, Nardo L, Baum T, Nevitt MC, McCulloch CE, Joseph GB, Lynch JA, Link TM.
I think there is a potential for prophylactic early interventions show extreme potential. The problem with neutrucueticals is the lack of regulation and inconsistencies with formulas. However, not enough is known about what occurs in the pathomechanisms of ANY intervention (drug or supplements). This would take extensive long term clinical trials on participants who do not have OA yet, but are at an increased risk to get it.
While there may be general assumptions made that the whole knee is susceptible for OA, the assumption is misleading and not well substantiated. The evolution of the OA lesion is almost always focal, beginning in a single joint compartment. The problem arises focally as a result of multiple factors which represent the imbalance between the most important mechanical factors, which are both dynamic (eg adduction moment) and static, (eg varus alignment), and biological (eg metabolic as alluded to above). Weak tissues are more susceptible, strong, well aligned limbs in slim individual are less at risk. Once the process starts all parts of the knee as joint structure become involved....the driving forces for progression are dominated by mechanical factors.
For more thoughts on this topic please visit www.oaisysmedical.com and look at 'Knee Pain; arthritis?"'
While I agree with Theodore and Robert, I do think that it is not just mechanical overload to blame. I think that etiology and progression is more a combination of the mechanical and chemical changes. Macro- and/or micro-traumatic loading causes biochemical changes within the joint. These biochemical changes can alter biomechanics and structural properties within the joint. (e.g., tissue that could normally withstand load and friction now becomes unable to). So it may not just be the mechanical overload that causes disease to progress, but the harsh biochemical environment in combination with the mechanical loading since it alters mechanical properties and thresholds.
The development of osteoarthritis is commonly seen following menisectomy in young patients and in some cases of advanced degenerative changes the menisci remain untouched. If the initial cartilage defect is the result of some basic mechanical or chemical background, further joint degeneration is the consequence of the same basic pathologies. In cases of traumatic chondral lesions, the size and the depth of the lesion probably will have the main role in development of subsequent changes.
There is no doubt that acute injury, especially meniscal injury, will result in OA in many patients. However, the cascade of events leading to joint degeneration is still unclear: focal, global, etc. Some recent unpublished data from my lab is looking in detail at some of these early changes in structure and biology that may elucidate the sequelae of joint disease caused by injury. That being said, we may also have some preliminary data to indicate the causes of so-called idiopathic OA, without previous joint injury. I think the important thing to keep in mind is that purely biological changes in the joint can lead to subsequent mechanical changes and vice versa which may lead to a negative feedback cycle of degeneration... I'm thinking specifically of PRG4 (lubricin) biochemical changes that can alter joint lubrication and lead to apoptosis and mechanical degradation (as an example of a plethora of similar associations). Thanks for the great post.
In etiological aspect there are different types of OA (at least 10): idiopathic, dysplastic, postarthritic, posttraumatic, postnecrotic (Perthes, Chandler), metabolic,etc. Grosso modo one can consider two main mechanisms for cartilage degeneration: either joint overloading in the presence of normal cartilage or abnormal cartilage (congenital metabolic insufficiency) in the presence of normal loading. Anyway, in my country we prefer the terminology "osteoarthrosis" which is more appropriate than "osteoarthitis" which is used in English-speaking countries. The ending "itis" corresponds to inflammatory process, and here we tackle a pathologic entity with a degenerative characteristics.