What Is OA (osteoarthritis)? Symptoms | Causes

What Is OA?

Osteoarthritis, also known as degenerative joint disease, is characterized by cartilage degeneration, a protective tissue found at the ends of the bones, resulting in structural and functional failure of synovial joints. Before we explore the specifics, it’s important to grasp the core concept of osteoarthritis.

Over time, cartilage wears down, rubbing together the ends of the bones, resulting in discomfort, restricted movement, and swelling. However, osteoarthritis is simply more than “wear and tear.” It is characterized by intricate cell connections, biochemical signals, and inflammatory reactions. Osteoarthritis disrupts the equilibrium of cartilage breakdown and repair.

 Normally, cartilage-forming cells, also known as chondrocytes, lay the material required for healthy cartilage. However, in OA, these chondrocytes are injured and become dysfunctional, resulting in the slow loss of cartilage.

Pathophysiology Of Osteoarthritis 

Now that you understand what is OA, it’s time to know the complex pathophysiology of this chronic condition.(2) However, to simplify this complex pathology, we need to know the structure of healthy joints and how OA affects them. The main components of joints are:

• Cartilage: serves as a protective tissue between bones, allowing smooth movement.
• Synovial fluid: provides lubrication to reduce friction.
• Subchondral bone: the layer of bone just under the cartilage.
• Ligaments and tendons: stabilize the joint.

In OA, the balance between cartilage degradation and synthesis is disturbed. The pathology of osteoarthritis is divided into two phases: early and late. 

Early OA

In early OA, chondrocytes work very hard to repair the damaged joint by proliferating and releasing inflammatory mediators, collagen (protein required for joints and bones), proteoglycans, and proteases and initiate secondary inflammatory changes in the synovial fluid and subchondral bone.

Late OA

In late osteoarthritis, repetitive injury and chronic inflammation result in chondrocytes drop out, marked loss of cartilage, and extensive subchondral bone loss. The degradation ultimately exceeds synthesis.

Here is the breakdown of the process:

Cartilage:

In OA, enzymes like metalloproteinases and inflammatory mediators like TGF-b, TNF, and prostaglandins damage the cartilage. Over time, the smooth surface roughness and the cartilage can wear away completely, resulting in bone-to-bone contact.

Subchondral Bone Changes:

As the cartilage erodes, the subchondral bone is exposed. It thickens and produces tiny growths known as bone spurs (osteophytes), which cause further discomfort and restrict movement.

Inflammation 

Unlike rheumatoid arthritis, although OA is considered a non-inflammatory disorder, it involves mild inflammation. According to various studies, moderate inflammation occurs in the synovial membrane, increasing pain and joint degeneration. (3) 

Synovial Fluid Changes 

As mentioned before, synovial fluids provide lubrication and minimize friction between bones. However, as the fluid composition changes, its lubrication capacity decreases, increasing joint stiffness.

This breakdown of joint tissue, combined with abnormal bone growth, leads to debilitating symptoms that characterize what is OA.

Symptoms of Osteoarthritis 

Osteoarthritis is an insidious disease. Recognizing the early warning symptoms of what is OA can help people seek treatment sooner and perhaps slow the disorder’s progression.

Joint Pain

Pain is among the most prevalent symptoms of OA. It can start as minor discomfort and progress to deep achy pain, especially after activity or at the end of the day. As the condition progresses, the pain can become persistent, even at rest.

The knee is most commonly involved, with a prevalence of 365 million. Unlike rheumatoid arthritis, OA affects large and weight-bearing joints like the knee, hip, lumbar spine, and cervical vertebrae.

Morning Stiffness 

Another distinguishing feature is stiffness, which occurs more often in the early morning. The joints may be difficult to move for thirty minutes after waking up.

Restricted Movements 

As the condition progresses, the range of motion in the afflicted joints reduces. People can struggle to fully bend or stretch their joints, especially the knees and fingers. 

Cracking Or Grating Sensation 

When moving the joint, it is normal to feel you are grinding or hear a cracking sound, commonly referred to as crepitus. This happens when the rough surface of the bones rub together.

Bone Spurs 

In some cases, bone spurs (osteophytes) can form surrounding the joint. These firm lumps can occasionally be felt beneath the skin and can impair mobility. Heberden’s nodes are felt at the tip of the finger or distal interphalangeal joint. Bouchard’s nodes are found at proximal interphalangeal joints. (4)

Causes of OA 

OA is a multifactorial disease; thus, there is no single cause. Instead, many variables contribute to the onset and progression of OA. Listed below are some of the most prevalent causes: 

Age 

Age is the most important risk factor for osteoarthritis. About 73% of people struggling with OA are older than 55. As people age, the cartilage in their joints gradually deteriorates, and then they become symptomatic.

Joint Injury 

As explained earlier, OA is a mechanical disease. It can be triggered by previous joint trauma, such as from sports, accidents, or repetitive stress. Trauma can alter the joint structure, increasing the susceptibility of osteoarthritis. 5,6

Genetics 

Some people may inherit a tendency to acquire the disorder if their parents or grandparents have osteoarthritis. More than 300 genomic loci have been identified to be associated with OA. (1)

Obesity 

Obesity also plays a role in OA. Carrying excess weight puts extra strain on weight-bearing joints. Obesity increases the 4 % risk of knee OA in women. (5) This increased pressure promotes cartilage breakdown in these joints.

Gender 

Females are more prone than males to get osteoarthritis, especially after age 50.(6) This can be attributed to hormonal changes after menopause, as estrogen has bone protective function.

Occupation And Lifestyle

Jobs that require repeated motions, such as kneeling, heavy lifting, or squatting, can raise the risk of OA. Overuse of weight-bearing joints accelerates cartilage wear and tear.

Metabolic Disorders 

Some metabolic disorders like diabetes and hemochromatosis, a disease in which the body absorbs excessive amounts of iron and deposits at various sites, including joints, have been related to an increased risk of OA.

Conclusion 

Understanding what is OA is the first step toward better management and early intervention. Recognizing what is 0A goes beyond viewing it as a natural consequence of aging; it is associated with various causes, clinical features, and detailed pathophysiology.

Addressing the risk factors early on and taking proactive steps can significantly improve the quality of life, even for those diagnosed with osteoarthritis.

References

1. WHO. (2023). Osteoarthritis. Retrieved from World Health Organization:
   https://www.who.int/news-room/fact-sheets/detail/osteoarthritisF
   
2. Shari M. Ling, M. (2020). Osteoarthritis: Pathophysiology. Retrieved from Hopkins Arthritis:
   https://www.hopkinsarthritis.org/arthritis-info/osteoarthritis/oa-pathophysiology/
   
3. Sokolove, J. (2013). Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations. Ther Adv Musculoskelet Dis. Retrieved from
   https://pmc.ncbi.nlm.nih.gov/articles/PMC3638313/
   
4. Ibrahim, D. (2024). Bouchard node. Retrieved from Radiopaedia:
   https://radiopaedia.org/articles/bouchard-node
   
5. JHAC. (2000s). Role of Body Weight in Osteoarthritis. Retrieved from Hopkins Arthritis:
   https://www.hopkinsarthritis.org/patient-corner/disease-management/role-of-body-weight-in-osteoarthritis/
   
6. Jaclyn McKenna, M. (2024). Why Women Are at Higher Risk for Getting Arthritis. Retrieved from HSS:
   https://www.hss.edu/article_women-and-arthritis.asp