Arthritis Glossary: A–Z Terms Explained

A

Adipokines

Hormone-like signalling proteins released by fat tissue, such as leptin, resistin and visfatin. Visceral (belly) fat releases more of the pro-inflammatory ones, which have been found in the joint fluid of people with osteoarthritis and rheumatoid arthritis.
See: Root Causes: metabolic dysfunction, Lifestyle & Toxins: visceral fat

Adiponectin

An adipokine with anti-inflammatory effects. Its levels tend to fall as visceral fat rises, removing a natural brake on inflammation.
See: Lifestyle & Toxins: visceral fat

Advanced glycation end-products (AGEs)

Harmful compounds formed when sugar binds to proteins without an enzyme, a process sped up by high blood sugar. In cartilage, AGEs cross-link collagen and make the tissue stiff and brittle.
See: Root Causes: metabolic dysfunction, Foods to Avoid: refined carbs

Anti-CCP antibodies

Antibodies against citrullinated proteins (anti-cyclic citrullinated peptide). They are a highly specific blood marker for rheumatoid arthritis and can appear years before symptoms; testing and interpretation belong with a physician.
See: Biomarkers: autoimmune markers

Arachidonic acid

An omega-6 fatty acid the body converts into inflammatory messengers such as prostaglandin E2 and leukotriene B4. Diets heavy in omega-6 oils are proposed to feed this cascade, a claim graded contested on this site.
See: Foods to Avoid: seed oils & trans fats, Anti-Inflammatory Plan: evidence for dietary interventions

Autoimmunity

When the immune system mistakenly attacks the body's own tissues. In autoimmune arthritis, such as rheumatoid or psoriatic arthritis, the joint lining is a main target.
See: Root Causes: autoimmune triggers

Autophagy

The cell's internal clean-up process, in which damaged parts are broken down and recycled. It is cited as one proposed benefit of medically supervised fasting.
See: Anti-Inflammatory Plan: evidence for dietary interventions

Avascular necrosis (osteonecrosis)

Death of bone tissue caused by a loss of blood supply, which can lead to joint collapse. It is a rare but recognized risk of long-term corticosteroid use.
See: Medications: corticosteroids

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B

Beta-casomorphin-7 (BCM-7)

A small opioid-like peptide released when A1 beta-casein from milk is digested. It is proposed to slow the gut and provoke gut inflammation; A2 milk does not release it. Its role in arthritis is contested.
See: Foods to Avoid: A1 vs A2 dairy

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C

C-reactive protein (CRP / hs-CRP)

A protein the liver makes in response to IL-6 and one of the most widely used blood markers of inflammation. The high-sensitivity test (hs-CRP) detects smaller, low-grade rises.
See: Biomarkers: inflammatory markers

Cartilage (articular)

The smooth, rubbery tissue that covers the ends of bones in a joint so they glide with little friction. It has no blood supply and relies on movement and its own cells (chondrocytes) for upkeep and repair.
See: Root Causes: nutrient deficiencies, Lifestyle & Toxins: sedentary behavior

Chondrocyte

The only cell type found in cartilage; it builds and maintains the cartilage matrix. Oxidative stress, inflammation and some drugs are proposed to damage chondrocytes or push them into programmed cell death.
See: Root Causes: oxidative stress

Citrullination

A chemical change in which the amino acid arginine in a protein is converted to citrulline. Citrullinated proteins can look foreign to the immune system and trigger the anti-CCP antibodies seen in rheumatoid arthritis.
See: Root Causes: autoimmune triggers, Biomarkers: autoimmune markers

Corticosteroids

Powerful anti-inflammatory drugs, such as prednisone, that mimic the hormone cortisol. They are valuable for severe flares, but long-term use is well documented to cause bone loss.
See: Medications: corticosteroids

Cortisol

The body's main stress hormone, released via the HPA axis. Short bursts reduce inflammation, but chronically high levels may impair bone remodelling and increase calcium loss.
See: Lifestyle & Toxins: stress & cortisol, Root Causes: hormonal imbalances

COX (cyclooxygenase)

Enzymes (COX-1 and COX-2) that turn fatty acids into prostaglandins. NSAIDs relieve pain by blocking them; curcumin and ginger are described as natural COX modulators.
See: Medications: the NSAID paradox

Curcumin

The main active compound in turmeric. It is studied for anti-inflammatory effects relevant to joints, though results vary by formulation and supplements should be discussed with a doctor.
See: Anti-Inflammatory Plan: integrative practitioners

Cytokine

A small protein that immune cells use to signal one another. Pro-inflammatory cytokines such as IL-6 and TNF-alpha drive much of the inflammation and cartilage breakdown in arthritis.
See: Biomarkers: inflammatory markers

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D

DAS28 (Disease Activity Score)

A standard score clinicians use to measure rheumatoid arthritis activity, based on 28 joints plus a blood test and the patient's own rating. Mediterranean-diet trials have reported improvements in DAS28.
See: Anti-Inflammatory Plan: evidence for dietary interventions

Diuretics (thiazide and loop)

"Water pills" such as hydrochlorothiazide and furosemide, used for high blood pressure and fluid overload. They can raise uric acid and are a recognized trigger of gout attacks.
See: Medications: drug-induced nutrient depletions

DMARD (disease-modifying antirheumatic drug)

A medicine that slows or stops the immune-driven joint damage of rheumatoid arthritis and related diseases, rather than only easing pain. Methotrexate is the usual first choice; biologic and targeted DMARDs are added if needed. Starting early matters.
See: Rheumatoid Arthritis: the window of opportunity

Dysbiosis

An unhealthy imbalance in the community of microbes living in the gut. It is proposed as an upstream driver of joint inflammation through the gut-joint axis.
See: Root Causes: gut-joint axis

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E

Eicosanoids

Signalling molecules made from fatty acids, including prostaglandins and leukotrienes. Those made from omega-6 arachidonic acid tend to promote inflammation, while omega-3s feed calmer pathways.
See: Foods to Avoid: seed oils & trans fats

Elimination diet

A structured trial in which a suspected trigger food is removed for a set window, often 30 to 60 days, then methodically reintroduced to see whether symptoms change. Best done with professional guidance.
See: Anti-Inflammatory Plan: evidence for dietary interventions, Foods to Avoid: nightshades

Endotoxemia

The presence of bacterial endotoxin (LPS) in the bloodstream. Low-grade endotoxemia from a leaky gut barrier is proposed to keep the immune system in a state of chronic inflammation.
See: Root Causes: gut-joint axis

Enthesis (enthesitis)

The spot where a tendon or ligament attaches to bone. Inflammation there, called enthesitis, is typical of spondyloarthritis and reactive arthritis, for example at the back of the heel.
See: Leaky Gut and Arthritis: reactive arthritis

Erythrocyte sedimentation rate (ESR)

A blood test measuring how fast red blood cells settle in a tube; inflammation makes them settle faster. It changes more slowly than CRP and is often read alongside it.
See: Biomarkers: inflammatory markers

Estrogen

A sex hormone that helps protect cartilage and the joint lining. Its decline at menopause is strongly associated with the rise in osteoarthritis among women.
See: Root Causes: hormonal imbalances

Evidence grades

The three badges this site uses on every major claim: Strong (broadly accepted), Emerging (promising but still developing) and Contested (disputed or not accepted by mainstream rheumatology).
See: About: how we grade evidence

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F

Fluoroquinolones

A class of broad-spectrum antibiotics, such as ciprofloxacin and levofloxacin. They carry an FDA boxed warning for tendinitis and tendon rupture.
See: Medications: fluoroquinolones

Fructose

A sugar found in fruit, table sugar and high-fructose corn syrup. Large amounts are processed in the liver in a way that raises uric acid, a well-established trigger for gout.
See: Foods to Avoid: sugar & HFCS

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G

Gliadin

A protein fraction of gluten that resists complete digestion. In susceptible people it is proposed to trigger zonulin release and increased gut permeability.
See: Foods to Avoid: gluten & wheat

Glycoalkaloids (alpha-solanine)

Natural compounds in nightshade vegetables such as potatoes and tomatoes. In a sensitive subset of people they are proposed to irritate the gut, though some studies also report anti-inflammatory effects.
See: Foods to Avoid: nightshades

Gout

A form of inflammatory arthritis caused by uric acid crystals forming in a joint, often the big toe, causing sudden, severe flares.
See: Foods to Avoid: sugar & HFCS, Biomarkers: metabolic markers

Gut-joint axis

The proposed two-way link between gut health and joint inflammation, in which gut microbes and the intestinal barrier influence immune activity in the joints. An active research area whose root-cause claims remain contested.
See: Root Causes: gut-joint axis

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H

Heavy metals

Toxic metals such as lead, mercury and cadmium. They are proposed to act as haptens, altering the body's proteins so the immune system attacks them; cadmium from cigarette smoke is a documented rheumatoid arthritis risk factor.
See: Lifestyle & Toxins: heavy metals

HLA-B27

A gene variant strongly linked to ankylosing spondylitis and related spondyloarthritis. In reactive arthritis it is associated with a more severe or long-lasting course, but a large population-based study found it did not predict who develops reactive arthritis after a gut infection.
See: Root Causes: autoimmune triggers

HLA-DRB1 (shared epitope)

A family of immune genes; certain versions carry a short protein sequence, the "shared epitope", linked to higher rheumatoid arthritis risk. Some bacterial proteins resemble this sequence.
See: Root Causes: autoimmune triggers

HOMA-IR

A calculation from fasting insulin and fasting glucose that estimates insulin resistance. It is an emerging, not yet routine, marker in arthritis care.
See: Biomarkers: metabolic markers

Homocysteine

An amino acid in the blood that reflects methylation, a process that depends on B vitamins. High levels are linked to oxidative damage and higher cardiovascular risk in rheumatoid arthritis.
See: Biomarkers: nutrient status

HPA axis

The hypothalamic-pituitary-adrenal axis, the brain-to-adrenal-gland system that controls cortisol release in response to stress.
See: Lifestyle & Toxins: stress & cortisol

Hyperuricemia

Abnormally high uric acid in the blood. It is the main risk factor for gout and can be driven by fructose, alcohol, purine-rich foods and some diuretics.
See: Biomarkers: metabolic markers, Medications: drug-induced nutrient depletions

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I

Iatrogenic

Caused by medical treatment. Medication side effects, such as diuretics raising uric acid, are a classic iatrogenic contributor to joint problems.
See: Medications

Inflammaging

The chronic, low-grade inflammation that tends to rise with age, partly driven by worn-out (senescent) cells. It is proposed as one link between ageing, metabolic disease and osteoarthritis.
See: Osteoarthritis: inflammaging

Insulin resistance

A state in which the body's cells respond poorly to insulin, so blood sugar and insulin stay high. It promotes AGE formation and inflammation linked to osteoarthritis and gout.
See: Biomarkers: metabolic markers, Root Causes: metabolic dysfunction

Interleukin-6 (IL-6)

A key pro-inflammatory cytokine with a strong pull toward joint tissue. It prompts the liver to make CRP and rises with gut permeability, poor sleep and excess visceral fat.
See: Biomarkers: inflammatory markers, Lifestyle & Toxins: sleep deprivation

Intestinal permeability ("leaky gut")

Loosening of the gut lining's tight seals so that bacterial products can pass into the bloodstream. Increased permeability is measurable, but "leaky gut" as a root cause of arthritis is contested.
See: Root Causes: gut-joint axis

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L

Leptin and resistin

Pro-inflammatory adipokines released in greater amounts by visceral fat. Both have been detected in the joint fluid of people with osteoarthritis and rheumatoid arthritis.
See: Lifestyle & Toxins: visceral fat

Lipopolysaccharide (LPS / endotoxin)

A molecule from the outer wall of certain bacteria that strongly activates the immune system. If it crosses a weakened gut barrier it can raise IL-6 and TNF-alpha throughout the body.
See: Root Causes: gut-joint axis

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M

Mast cells

Immune cells that release histamine and other inflammatory chemicals when triggered. Nightshade compounds are proposed to activate gut mast cells in sensitive people.
See: Foods to Avoid: nightshades

Matrix Gla Protein (MGP)

A protein that stops calcium from depositing in soft tissue and cartilage. It needs vitamin K2 to become active.
See: Root Causes: nutrient deficiencies

Matrix metalloproteinases (MMPs)

Enzymes that break down collagen and other parts of the cartilage matrix. Oxidative stress, low vitamin D and fluoroquinolones are proposed to increase their activity.
See: Root Causes: oxidative stress, Medications: fluoroquinolones

Mediterranean diet

An eating pattern rich in vegetables, olive oil, fish, legumes and whole grains. It has the strongest evidence of any diet on this site for lowering hs-CRP and improving rheumatoid arthritis activity.
See: Anti-Inflammatory Plan: evidence for dietary interventions

Molecular mimicry

When part of a microbe or food protein closely resembles a human protein, so the immune response aimed at the invader also attacks the body's own tissue. A proposed trigger of autoimmune arthritis.
See: Root Causes: autoimmune triggers

Mycotoxins

Toxic compounds produced by moulds, for example in water-damaged buildings. They are proposed to disrupt the gut barrier and keep the immune system activated; their role in arthritis is contested.
See: Lifestyle & Toxins: mold mycotoxins

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N

Nightshades (Solanaceae)

The plant family that includes tomatoes, potatoes, peppers and aubergine (eggplant). Whether they worsen arthritis is contested and appears highly individual.
See: Foods to Avoid: nightshades

NSAID

Nonsteroidal anti-inflammatory drug, such as ibuprofen, naproxen or diclofenac. They relieve pain by blocking COX enzymes; a contested claim holds that long-term use may slow cartilage repair.
See: Medications: the NSAID paradox

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O

Omega-6 to omega-3 ratio

The balance between omega-6 fats (mainly linoleic acid from seed oils) and omega-3 fats (EPA, DHA and ALA from fish, flax and walnuts). A high ratio is proposed to favour inflammation, though whether seed oils inflame humans is contested.
See: Foods to Avoid: seed oils & trans fats, Anti-Inflammatory Plan: integrative practitioners

Osteoarthritis (OA)

The most common form of arthritis, involving cartilage loss and changes to the underlying bone. Long framed as "wear and tear", it is increasingly linked to metabolic and inflammatory drivers.
See: Root Causes: metabolic dysfunction

Oxidative stress

An imbalance in which reactive oxygen species outpace the body's antioxidant defences, damaging cells and tissues. In joints it is proposed to harm chondrocytes and speed cartilage breakdown.
See: Root Causes: oxidative stress

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P

Porphyromonas gingivalis

A gum-disease bacterium and the only known microbe that makes the enzyme PPAD, which citrullinates proteins. It is proposed as a link between periodontitis and rheumatoid arthritis.
See: Root Causes: autoimmune triggers

Prostaglandin E2 (PGE2)

A messenger molecule made by COX enzymes that drives pain and inflammation but is also described as signalling cartilage repair. NSAIDs reduce it.
See: Medications: the NSAID paradox, Foods to Avoid: seed oils & trans fats

Proton pump inhibitors (PPIs)

Acid-reducing drugs such as omeprazole. Long-term use is strongly linked to low magnesium and can also reduce vitamin B12 and calcium absorption.
See: Medications: drug-induced nutrient depletions

Purines

Natural compounds in foods such as red and organ meats, some seafood and beer. The body breaks them down into uric acid.
See: Foods to Avoid: alcohol, red meat & caffeine

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R

RAGE

The receptor for advanced glycation end-products, found on cartilage and immune cells. When AGEs bind it, it triggers inflammatory signalling inside the joint.
See: Root Causes: metabolic dysfunction

Reactive arthritis

Joint inflammation that appears one to six weeks after a gut or urinary-genital infection, such as Salmonella or Chlamydia. Most cases settle within months; carrying the HLA-B27 gene variant is linked to a more severe or chronic course.
See: Root Causes: autoimmune triggers

Reactive oxygen species (ROS)

Unstable, oxygen-containing molecules produced during normal metabolism and immune activity. In excess they cause oxidative stress.
See: Root Causes: oxidative stress

Rheumatoid arthritis (RA)

An autoimmune disease in which the immune system attacks the joint lining, causing pain, swelling and, over time, joint damage. It usually affects joints on both sides of the body.
See: Root Causes: autoimmune triggers

Rheumatoid factor (RF)

An autoantibody that targets the body's own antibodies. It is a classic rheumatoid arthritis marker but less specific than anti-CCP and can appear in other conditions.
See: Biomarkers: autoimmune markers

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S

Seronegative

Describes inflammatory arthritis in which the usual blood antibodies, such as rheumatoid factor or anti-CCP, are not detected.
See: Lifestyle & Toxins: mold mycotoxins

Specialized pro-resolving mediators (SPMs)

Molecules made largely from omega-3 fats that actively switch off an inflammatory response once its job is done, rather than merely suppressing it.
See: Anti-Inflammatory Plan: evidence for dietary interventions, Root Causes: nutrient deficiencies

Subchondral bone

The layer of bone directly beneath joint cartilage. Its health affects how loads pass through the joint, and it can be weakened by chronic cortisol or long-term corticosteroids.
See: Root Causes: hormonal imbalances, Medications: corticosteroids

Synovium and synovial fluid

The synovium is the thin membrane lining a joint; it produces synovial fluid, which lubricates and nourishes cartilage. Inflammation of the synovium (synovitis) is central to rheumatoid arthritis.
See: Root Causes: gut-joint axis, Lifestyle & Toxins: sedentary behavior

Synovitis

Inflammation of the synovium, the thin lining of a joint. It is the main feature of rheumatoid arthritis, and milder, low-grade synovitis is common in osteoarthritis and linked to pain.
See: Osteoarthritis: low-grade synovitis

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T

Th17 cells and Tregs

Two types of T cells: Th17 cells promote inflammation, while regulatory T cells (Tregs) calm it. A shift toward Th17 dominance is reported in several forms of inflammatory arthritis.
See: Root Causes: gut-joint axis

TNF-alpha

Tumour necrosis factor-alpha, a pro-inflammatory cytokine that drives cartilage breakdown in the joint. It is the target of several biologic drugs for rheumatoid arthritis.
See: Biomarkers: inflammatory markers

Tophi

Chalky lumps of uric acid (urate) crystals that build up in and around joints, tendons or the ear after years of untreated high uric acid. Keeping uric acid low with treatment can shrink them.
See: Gout: urate-lowering therapy

Trans fats

Industrially produced fats from partially hydrogenated oils. They are well documented to increase inflammation and oxidative stress.
See: Foods to Avoid: seed oils & trans fats

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U

Uric acid

A waste product formed when the body breaks down purines and fructose. High levels can crystallize in joints and cause gout, and may also act as a broader inflammatory signal.
See: Biomarkers: metabolic markers, Foods to Avoid: sugar & HFCS

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V

Visceral fat

Fat stored deep in the abdomen around the organs. It acts like a hormone-producing organ, releasing inflammatory adipokines that can affect joints independent of mechanical load.
See: Lifestyle & Toxins: visceral fat

Vitamin D (25-hydroxyvitamin D)

A vitamin that acts like a hormone in immune regulation and bone health; blood levels are measured as 25-hydroxyvitamin D. Deficiency may worsen autoimmune activity and cartilage breakdown.
See: Biomarkers: nutrient status

Vitamin K2

A form of vitamin K (menaquinone, including MK-7) that activates Matrix Gla Protein to keep calcium out of cartilage. It can interact with blood thinners, so discuss with a doctor.
See: Root Causes: nutrient deficiencies

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Z

Zonulin

A protein that regulates the tight seals between gut-lining cells. Gliadin from gluten is proposed to trigger zonulin release, increasing intestinal permeability.
See: Foods to Avoid: gluten & wheat

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