14. Better views on Obesity and Osteoarthritis

Obesity + Osteoarthritis(OA)

As we’d discuss in this short post is a mind-numbingly complex entity where surety, predictions, and conclusive statements are a definite no-no! And the ‘uncertain’ psychosocial factors that are rarely considered to be a part of the ‘developmental process’ of OA might as well be equally contributory as biological and mechanical factors. 

Maybe even priming the biology towards a disease state….?

To avoid confusion and repetitiveness; unless specified, most of the stuff in the blog would be revolving around knee osteoarthritis.

Let’s begin by defining OA:

Osteoarthritis is classically defined by popular internet media, and clinicians, mostly characterize it as a disease of ‘wear & tear’ type of joint inflammation. Wherein your joint surface cartilage just erodes with time(age) much like soil erosion in plains.

Which in my opinion is a great way to visualize how patients assume the insides of their knees look when told about the ‘wear & tear’.

Is there a better way to look at OA?

While the diverse appearance of the primary risk factors (aging, obesity, and trauma) for developing OA suggests that there are multiple pathways to the disease, the fact that the state of the disease can be characterized by a broad scope of biopsychosocial, structural and mechanical components calls for a revaluation of how we fundamentally understand Osteoarthritis as clinicians.

For example; OA has been characterized as a disease of mechanics, and genetics, a disease that is driven by aberrant joint structure and morphology as well as a disease substantially influenced by inflammatory mediators. (here)

It still isn’t as simple as literary definitions of these contributory/risk factors.

Isn’t OA an inflammatory disease?

Yes! Osteoarthritis is an inflammatory disease of the joint (as an organ), studies have reported elevated ESR and serum + intra-articular levels of Proinflammatory Cytokines: IL-6, IL-10, TNF-𝛼 (and TNF-𝛼 soluble receptors sTNFR1 and sTNFR2, and C-reactive protein, and IL-1𝛼 & IL-1𝛽) and MMP family of proteases. (here)

And *Anti-inflammatory Cytokines IL-10.

That being said, Not all Osteoarthritis patients are/present the same. Not even close! thus ‘disease of joint as an organ’ (here)

Just to dip an explanatory toe in:

1. Driven by mechanical factors(injury/trauma to structures in and around the knee joint), OA is an active response to injury, rather than a degenerative process in some.

2. Considering aging, OA might as well be secondary to a trigger/contributory factor (injury, stress, trauma) superimposed on a chronic, sterile, low-grade inflammation or INFLAMMAGING!

3. Considering obesity and loading: (discussed in the next section)

Let’s try to keep it simple.

Is the ‘wear & tear’ definition wrong? Yes!

Partly because it’s an inaccurate interpretation/understanding of the pathogenesis of Osteoarthritis and its correlation to joint loading. and

Partly because it is linked to a host of nocebic mumbo-jumbo and ‘advice/restrictions’ that instill fear, fragility, and mechanistic narratives among patients and the general population.

Coming to Obesity and Osteoarthritis. To further explain said points:

In a perfect world, we’d be sensitive enough to realize & normalize by now, the fact that obesity is not a ‘choice’ and it doesn’t lead to OA as mechanically as we think.

Defining & Associating it with OA; simply based on biomedical terms and correlations is unfair and is probably a big hurdle in the way of proper management of either condition.

Obesity(causes of obesity) and OA are complex entities by themselves, products of genes and environments and various modifiable and non-modifiable factors.

Quite poetic is the fact that; while Obesity is one of the few modifiable factors in osteoarthritis, obesity affects how we manage OA, and similarly, OA affects how we manage obesity. (here)

What’s the problem then?

1. BMI is an unfair estimate of how much fat someone carries (adiposity), especially in populations with high lean muscle mass. It is used quite extensively in research due to the simple fact that ‘it is easy to use.‘

2. Historically, the high incidence of knee OA in obese people led to the assumption that the link was purely mechanical: excessive weight increases joint loading, resulting in wear and tear of joints. Thus, it is still believed that increased body weight increases joint reaction forces and malalignments, which in turn increases wear on the cartilage and are predictors of disease progression.

1. My first concern with this belief is that it is unknown whether these ‘malalignments’ precede or follow OA? (or whether they are just adaptive changes)
   

2. My second concern is; How the reductionist & mechanical association between OA and Obesity still stands, when it fails to explain how the odds of OA in NWB(non-weight-bearing) regions such as hands also increase with increased BMI (&/or obesity) (here)

SO!, it’s all fake? Loading has nothing to do with OA?

Not exactly, joint Biomechanics and Osteoarthritis have a much more complex relationship than we care to acknowledge.

To explain:

Animal studies have shown that abnormal loading (rate, time, and/or force) and mechanoreceptor activation can indeed change cartilage metabolism and chondrocyte inflammatory state in a way that eventually results in cartilage degradation.

It just isn’t the ‘load will scrape your joint off’ kind of association.

The missing links?

1. The abnormal lipid profile or Dyslipidaemia.

Characterized by high plasma levels of TGs, low levels of HDL-c, often slightly increased levels of LDL-c, and increased levels of FFAs.

Low levels of HDL-c and high levels of Ox-LDL and FFAs Have been shown to play a role in the loss of protective mechanisms, activation of certain cartilage destructive factors, macrophages, and aggravation of inflammation in synovium and cartilage, and proteoglycan loss in articular cartilage. Producing additional synovitis which in turn loops back to make things even more inflammatory and ‘generally worse’.

2. Low-grade Systemic and Local Inflammation:

A low-grade inflammatory state in the body caused by obesity is primarily due to excess adiposity. Specifically White adipose tissue (WAT). Which is found in abundance in obese individuals. Adipose tissue is also a powerful endocrine organ that secretes a variety of pro/anti-inflammatory and immunomodulatory cytokines,

1. Which can help us understand the 2x increased risk of Hand OA with obesity (systemic factors released mainly by adipose tissue reach and then activate joint cells.)

2. Considering local inflammation (Infrapatellar fat pad) IPFP could play a local in the production of inflammatory cytokines/adipokines in knee OA.

3. Post-menopausal OA could be (although with extreme caution) attributed to loss of the inhibitory effect of estrogen and ovarian function on the secretion of proinflammatory cytokines as well.

4. These systemic inflammatory processes are also hypothesized to be drivers of many systemic conditions that present with Obesity apart from OA, a cluster of conditions like Alzheimer’s, hypertension, insulin resistance, and atherogenic dyslipidemia.

3. Obesity in itself could lead to pain!

Obesity is a strong independent risk factor for pain, nearly doubling the risk of chronic pain in the elderly after adjusting for insulin resistance, inflammation, and pain-related comorbidities.

(generalized MSK pain syndromes, fibromyalgia,post-surgical complications & dissatisfaction, decreased Quality of life & participation restrictions, Chronic stress, emotional and psychosocial irregularities)

(here) (here) (here)

To conclude:

Osteoarthritis is more than just ‘wear & tear’. In fact, it’d be more accurate to say ‘complicated and degenerated’.

All we can take away from here is;

1. Your weight isn’t crushing your joint into damage

2. It’s more systemic and subtle than you explain to patients/ have been explained by your doctor.

3. Considering/advising weight loss is great! Leaving people hanging with just the advice isn’t.

4. Exercise is both safe and good for your joints (with a few exceptions).

5. OA isn’t simple, evidence suggests that osteoarthritis is a systemic disorder of multifactorial origin, wherein genetic, environmental, hormonal, and metabolic factors interact and contribute to the initiation and evolution of the disease.

So, its explanation shouldn’t be reductionist, mechanical, or straightforward at all!

Disclaimer: In the presence of pain all the structures and context must be clinically assessed, this blog is in no way a substitute for a clinical assessment and all must consult a physiotherapist or a physician in such conditions.

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