Spinal arthritis, also known as arthritis of the back or neck, refers to inflammation affecting the facet joints in the spine as well as other spinal structures. What exactly triggers this inflammation depends on the type of spinal arthritis present.

Types of Spinal Arthritis

Osteoarthritis

Osteoarthritis, the most prevalent type of spinal arthritis, arises from general wear and tear on the joints over time. The cartilage acting as a cushion between joints slowly deteriorates, allowing bone to rub against bone. This causes inflammation and pain.

Osteoarthritis frequently appears in the facet joints linking vertebrae in the neck and lower spine. As spinal discs degenerate, more pressure transfers to facet joints, worsening the erosion of cartilage. Genetics play a role as well. Past back injuries also raise osteoarthritis risk later on.

Over 50% of people above age 65 show some osteoarthritis on x-rays. It affects more men under 45 but more postmenopausal women.

Rheumatoid Arthritis

The immune system attacking the joint lining – called synovium – leads to rheumatoid arthritis. It too may provoke spinal inflammation, especially in the cervical vertebrae. Women suffer rheumatoid arthritis more often than men.

Unlike osteoarthritis stemming from mechanical damage, rheumatoid arthritis flares up independently of physical activity, causing spontaneous back pain.

Spondyloarthritis

This umbrella term covers inflammatory spinal arthritis unrelated to rheumatoid arthritis. Various forms exist:

• Ankylosing spondylitis: Inflammation of vertebrae and sacroiliac joints potentially progressing to spinal fusion
• Psoriatic arthritis: Associated with the autoimmune skin condition psoriasis
• Reactive arthritis: Joint inflammation following infection elsewhere in the body
• Enteropathic arthritis: Arthritis linked with inflammatory bowel disease

In essence, spondyloarthritis involves both joint and enthesis inflammation, where ligaments/tendons attach onto bones. Genetic factors contribute, as do some infections and immune disorders.

Main Causes and Risk Factors

Advancing age prominently correlates with developing spinal arthritis, especially osteoarthritis. Studies show at least 50% of senior citizens display some spinal arthritis.

Genetics also raise susceptibility. Researchers have identified inherited osteoarthritis and spondyloarthritis genes.

Carrying excess weight adds substantial stress to back joints and ligaments, expediting injury alongside spinal arthritis. Losing even a few pounds can dramatically alleviate arthritis symptoms.

Prior trauma to the joints, ligaments or spinal cartilage predisposes individuals to spinal arthritis later on, even years after initial damage seemingly heals. Repetitive overuse of the back especially while lifting or bending further worsens existing inflammation.

Certain uncommon bone deformities present from birth make joint damage and arthritis more likely.

Anatomical Predispositions

Variations in spinal architecture like scoliosis or stenosis place uneven pressures on vertebral bones and surrounding tissues, raising arthritis likelihood. Old vertebral fractures also alter load distribution and joint mobility, potentiating localized wear and tear.

Systemic Inflammation

Disorders like diabetes, autoimmune conditions, atherosclerosis and gout create higher background inflammation and circulation abnormalities that appear to exacerbate cartilage erosion and arthritis progression.

Inherited Traits

Genetic mutations linked to joint formation/repair processes predispose individuals to cartilage defects and early-onset degeneration. Having close family members with spinal arthritis also heightens personal risk, highlighting genetic contributions.

How Does Spinal Arthritis Develop?

Here’s an overview of the step-wise physical processes spurring arthritis inside spinal joints:

1. Early Cartilage Damage

The slippery cartilage coating the ends of facet joints permits smooth gliding movement. But sustained overloading causes microtears and surface abrasions. Enzymes begin degrading the cartilage matrix. Inflammation brews.

2. Accelerating Breakdown

Cartilage damage accumulates with continued use. The cartilage loses elasticity and the ability to distribute pressures evenly across joint surfaces. Unprotected bony surfaces start grinding, releasing debris that inflames nearby tissues.

3. Bone Changes

In response to destabilized, painful joints, the body floods affected areas with immune cells and ramps up localized bone growth. Bony spurs form as bone tries to brace damaged regions. Misguided remodeling attempts lead to arthritis progression.

4. Nerve Irritation

Expanding, inflamed facet joint tissues begin compressing spinal nerves. Bulging, injured discs can further pinch delicate nerves, eliciting pain signals. Chronic compression alters nerve function.

5. Biomechanical Shifts

Spinal arthritis severely alters joint mobility. Stiff, rigid segments transfer more shearing forces onto vulnerable transition zones in efforts to maintain overall flexibility and motion. This strains adjacent joints, propagating arthritis downward like a domino cascade through the spine.

Additional Contributors

Below are some secondary factors that might also play into arthritis risk:

Nutritional Deficits

Diets low in anti-inflammatory compounds and collagen-building blocks like vitamin C, vitamin D, magnesium and omega-3 fatty acids negatively impact skeletal health. Antioxidant shortages permit excess joint inflammation and damage.

Poor Circulation

Atherosclerosis and reduced microvascular supply choke flows to joint tissues, compounding inflammatory and degenerative processes. This slows waste removal and nutrient delivery, further impairing homeostasis.

Hormonal Changes

Marked hormonal transitions in life phases like menopause and andropause modify inflammatory balances and connective tissue compositions in complex ways not fully elucidated. Hormone imbalances may leave joints more vulnerable.

Microbes and Viruses

Some research indicates that certain bacteria or viruses may play initiating or amplifying roles in arthritis progression. However, how infection might spark joint deterioration requires clarification.

Emotional Stress

Mental distress creates physiological changes spurring systemic inflammation and tissue degeneration. It also modifies pain perception pathways. Minimizing distress, depression and anxiety helps some arthritis patients.

Complications

As spinal arthritis advances, bony protrusions called osteophytes or more commonly referred to as bone spurs, often emerge along joint edges as facet joints enlarge. Research shows up to 30% of spinal arthritis patients develop bone spurs. Although not directly harmful, bone spurs narrow openings for exiting nerve roots. This pinches nerves, producing:

• Spinal stenosis: Here, bone spurs and swollen facet joints narrow the spinal canal itself. One study found a 13% spinal stenosis rate among spinal arthritis patients over age 60. Symptoms include back pain, numbness, tingling, and weakness from spinal cord compression.
• Radiculopathy: Pressure on nerve roots exiting the spine triggers painful radiculopathy. For example, sciatica results when a herniated disc or bone spur compresses the sciatic nerve. 40% of radiculopathy cases stem from spinal osteoarthritis.

The inflammatory spinal arthritis subtype ankylosing spondylitis promotes growth of fibrous spinal tissue and new bone formation. Over time, this fuses vertebrae together in a hunched, immobilized position. Complete spinal fusion occurs in up to 28% of these patients. Fused vertebrae easily crack and fracture. One study saw a 36% vertebral fracture rate in advanced ankylosing spondylitis. Rarely, the rigid spine collapses under pressure.

Conclusion

Basically, there are a whole bunch of different factors that can lead to spinal arthritis, and these causes are complex and vary quite a bit person-to-person. But some clear common threads emerge – years of excessive mechanical stress on the spine, injuries that never properly heal, inflammation run amok, and inherited genetic glitches can all pile up to gradually chip away at the super slick cartilage pads cushioning spinal bones. Bit by bit, this irreplaceable cartilage gets so damaged that it provokes widespread joint degeneration. The good news is that catching things early and attempting to dial back these damaging drivers where possible may help prevent severe arthritis from taking hold throughout the spine..