Arthritis – Osteoarthritis
Osteoarthritis is a very common degenerative joint disease and a leading cause of disability. Affecting over 20 million in the U.S. alone, this progressive disease is characterized by structural damage and functional impairment within joints (CDC 2012; NIH MedlinePlus 2012; Mayo Clinic 2012; Seed 2011; Lawrence 2008; Lane 2011).
Many interrelated factors – such as obesity and oxidative stress – work together in osteoarthritis to cause progressive, degenerative changes in weight-bearing joints including the knees, neck, lumbar spine, and hips, as well as the hands. A multifactorial approach is best when targeting osteoarthritis management (Ziskoven 2011; Busija 2010).
Conventional medical treatment focuses upon reducing load (e.g. weight loss) and improving joint support (i.e. enhancing muscle strength), as well as treating the pain and stiffness of osteoarthritis with acetaminophen and other NSAID drugs.
However, these drugs expose arthritis sufferers to the risks of liver and kidney damage (Woodcock 2009). In addition, these drugs often offer only incomplete/ partial relief (Vista 2011; Bijlsma 2011), and treatment with acetaminophen and NSAIDs fails to help the body rebuild damaged joint cartilage (Kapoor 2011).
On the other hand, natural compounds like undenatured type-II collagen and methylsulfonylmethane (MSM) modulate fundamental aspects of osteoarthritis pathology, while others such as krill oil and Boswellia serrata target novel inflammatory pathways that can contribute to pain, swelling and joint degradation (Min 2006; Wang 2004; Palmieri 2010; Gregory 2008; Deutsch 2007; Sengupta 2010; Sengupta 2011).
Upon reading this protocol, you will learn about the critical medical factors of osteoarthritis, as well as learn about some underappreciated, yet potentially dangerous side effects of drugs often used to treat osteoarthritis pain. Additionally, you will discover several natural treatment strategies that have been shown to help support joint structure and function to provide more than just pain relief.
Arthritis – Osteoarthritis Understanding Osteoarthritis
Normal Joint Anatomy and Function
The bones of the human skeletal system are connected by a complex series of joints, which connect two or more bones and allow for a wide variety of movements that would otherwise be impossible (Briant 2008).
In order to facilitate smooth joint movement, the surfaces of joints are lined by a low-friction, load-distributing, wear-resistant tissue called articular cartilage, which is composed of 65 to 80 percent water, collagen (fibrous proteins), proteoglycans, and chondrocytes (cells that produce cartilage) (Pearle 2005). In adults, damaged cartilage has a very limited capacity for self-healing due to blood supply limitations, and the relatively poor capacity of resident chondrocytes to migrate and proliferate (Henrotin 2009).
Joints can be classified as synovial, fibrous, or combination joints, based on the presence or absence of a synovial membrane and the amount of motion that occurs in the joint.
Normal synovial joints allow a significant amount of motion the articular surface. These joints are composed of the following:
- Articular cartilage
- Subchondral bone
- Synovial membrane
- Synovial fluid
- Joint capsule
Normal articular surface of synovial joints consists of articular cartilage surrounded by proteoglycans and collagen. The cartilage protects the underlying subchondral bone by distributing large loads, maintaining low contact stresses, and reducing friction.
Synovial fluid supplies nutrients to the articular cartilage; it also absorbs shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.
Osteoarthritis Onset and Progression
Osteoarthritis (OA) can occur in any freely moving joint in the body, but it most commonly affects load- and stress-bearing joints like the knees, lumbar spine, and hips (Lawrence 2008).
At the onset of OA, where cartilage cells depart from their normal pattern of growth and differentiation, the outermost layer of articular cartilage begins to soften as its protein structure degrades. As OA progresses, this loss of protein content becomes more rapid, affecting deeper and deeper layers of cartilage (Pearle 2005). Eventually, the entire protective layer of cartilage is destroyed as the chondrocytes become completely overwhelmed and unable to reverse the tissue damage.
Because cartilage does not contain free nerve endings, joint destruction is typically not associated with pain until it is considerably advanced. This is a major reason why OA tends to be diagnosed so late in the disease process (Bijlsma 2011; Felson 2005).
With a majority of the protective cartilage now gone, the raw surfaces of the bones become exposed to gradual bone-on-bone erosion. This process inevitably leads to the destruction/deformation of nearly all the joint structures involved in movement, and is often accompanied by chronic inflammation in and around the joint space (i.e., synovial membrane) (Pearle 2005).
In many cases, the bone destruction caused by OA is followed by “remodeling”, which is characterized by bone spurs that grow along the joint margins. Although these bony outgrowths are believed to stabilize the injured joint by increasing bone surface area, they are also a significant source of pain, as joint movement causes them to rub against adjacent bones, nerves, and/or soft tissue (Mayo Clinic 2009; Pearle 2005). The intensity of symptoms can vary significantly, ranging from mild to severe (Strand 2011).
The pain caused by OA is typically worsened upon physical activity. As the disease progresses, however, patients may begin to report pain even when resting. Complaints of stiffness tend to occur more frequently in the morning, and often resolve shortly after awakening. However, any period of prolonged inactivity can cause this stiffness, which is sometimes referred to as “inactivity gelling” (Kalunian 2012b).
In cases of advanced OA, patients often report both physical and psychosocial disability. In fact, along with cardiovascular disease, OA causes more disability than any medical condition among the elderly (Hunter 2009).
Arthritis – Osteoarthritis
Osteoarthritis Causes and Risk Factors
Osteoarthritis (OA) arises as a result of a complex interplay of factors such as aging, mechanical forces, joint integrity, local inflammation, genetics, and congenital abnormalities (Kalunian 2012a; Bijlsma 2011).
Risk factors for osteoarthritis include (Seed 2011; Busija 2010):
- Advanced age
- Female gender
- Obesity (see below)
- History of physical labor
- High-impact sports
- Joint trauma
- Family history
Obesity and Osteoarthritis
Because obesity increases the load and stress on many joints, it appears to be one of the most influential risk factors contributing to the development or advancement of osteoarthritis (OA) (Busija 2010). However, studies of obese patients have identified a high prevalence of OA in non-weight bearing areas (e.g., finger joints) as well (Rai 2011).
Data reveal that fat tissue is a major source of catabolic and pro-inflammatory mediators (i.e., cytokines, chemokines, and adipokines), which are implicated in the process of OA (Rai 2011). In addition, obese patients tend to experience insulin resistance and increased glucose load, which may also contribute to the chronic inflammation and cartilage degradation of OA (Sowers 2010).
Since OA has been linked not only to obesity, but also to other cardiovascular risk factors (e.g., diabetes, dyslipidemia, hypertension, and insulin resistance), researchers have proposed that it might be related to a much larger group of risk factors, called “metabolic syndrome” (Velasquez 2010; Katz 2010).
Recent studies have shown that physical activity and diet programs (alone or in combination) are associated with a reduction in pain, as well as functional improvement among overweight or obese adults with OA (Brosseau 2011). In cases where patients are too obese to engage in physical activity, bariatric surgery has also been correlated with improvements in pain and function among patients with OA of the hip and knee (Gill 2011).
Metabolic Factors Associated with Osteoarthritis
Several interrelated metabolic factors also contribute to osteoarthritis onset and progression; chief among which are inflammation, mitochondrial dysfunction, and oxidative stress.
- Inflammation – Osteoarthritis (OA), like many other age-related diseases, is tied to excessive inflammation (Goldring 2011).Over-indulgence in foods rich in pro-inflammatory omega-6 fatty acids and insufficient intake of foods rich in anti-inflammatory omega-3 fatty acids characterizes the dietary pattern of most modern, industrialized nations.Arachidonic acid (an omega-6 fatty acid) is the raw material used by the body to synthesize numerous inflammatory mediators, including leukotriene B4, prostaglandin E2, and thromboxane A2, all of which contribute to pain, swelling, and joint destruction (see figure 1) (Liagre 2002; Devillier 2001; Kawakami 2001).
- Mitochondrial dysfunction – Mitochondria are the power cores of our cells; they generate the energy that cells need to function. With age, mitochondrial function deteriorates, leading to a variety of negative consequences (Vaamonde-Garcia 2012; Cillero-Pastor 2008; Blanco 2004).In the case of OA, dysfunctional mitochondria conspire with inflammation to augment joint destruction. One study found that the inflammatory propensity of chondrocytes was amplified when their mitochondria were dysfunctional. Specifically, mitochondrial dysfunction in chondrocytes is associated with increased reactive oxygen species production and activation of the “master-regulator” of inflammation, nuclear factor-kappa B (Nf-kB) (Vaamonde-Garcia 2012).Fortunately, adhering to a plant-based diet rich in dietary antioxidants, reduced in saturated fat, and balanced in omega-6 and omega-3 fats, such as the Mediterranean diet (see Nutritional Interventionssection below) may be an effective means of targeting several of the metabolic imbalances that affect OA.
- Oxidative stress – Oxidative stress, which is caused by free radicals, is known to be a factor in cartilage destruction and inflammation. These reactive molecules are also involved in pain perception (Ziskoven 2010).
Hormones and Osteoarthritis
After the age of 50, more women are affected by osteoarthritis (OA) than men (Bijlsma 2011); this female preponderance suggests that hormone abnormalities may influence the progression and development of the disease (Tanamas 2011).
The link between hormones and OA is further supported by evidence linking hormone (e.g., estrogen) deficiencies to an increased risk of osteoarthritis (Parazzini 2003).
In addition, some evidence suggests that hormone replacement therapy can relieve symptoms of OA, especially among postmenopausal women (Song 2004). As a result, Life Extension encourages OA patients to test for hormone deficiencies and correct them when identified.
Further reading is available in the Female Hormone Restoration protocol.
(Aldamiz-Echevarria 2007; Wixted 2010; Simopoulos 2011; Schror 2011; Bengmark 2006; Murias 2004; Oz 2008; Keicher 1995; Prasad 2004; Safayhi 1992)
Arthritis – Osteoarthritis
Osteoarthritis (OA) is diagnosed based upon medical history and clinical examination (Busija 2010).
Radiographic imaging can aid in the diagnosis of OA. It involves the identification of a variety of anatomic abnormalities such as joint space narrowing, bone spurs, and joint bone deformity (Murphy 2012). However, since many patients with joint abnormalities do not develop symptoms, a diagnosis of OA cannot be made solely upon the basis of positive radiographic images. Likewise, patients with symptoms of OA may not display radiographic evidence (Bijlsma 2011).
A newer method of imaging called delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) provides information about cartilage quality and may offer an improved means of diagnosing OA in the early stages (Siversson 2012). This method involves the intravenous injection of a negatively charged contrast agent, which then diffuses into articular cartilage over at least two hours. An increased concentration of contrast agent (in positively charged areas on the MRI scan) would be indicative of articular cartilage damage in that specific region (Taylor 2009). READD MORE HERE ……..