NU 245 · NursingSection 2.8 · Musculoskeletal and skin disorders

Section 10 of 18

Osteoarthritis and rheumatoid arthritis

Explain why osteoarthritis and rheumatoid arthritis both damage joints but by different mechanisms, tell the two apart from the pattern of joints and symptoms each produces, and describe the treatment principle that follows from each cause.

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Why this matters

Joint pain is one of the commonest reasons a patient seeks care, and these two diseases account for most of it. They are easy to blur together because both cause pain, stiffness, swelling and deformity, yet they behave differently, affect different tissues, carry different risks outside the joint and need different medicines. A patient with rheumatoid arthritis who is treated as though she had osteoarthritis loses joint tissue that early disease-modifying treatment could have saved, while a patient with osteoarthritis who is given powerful immunosuppression takes on infection risk for no benefit. Learning the mechanism and the pattern behind each disease is what lets you question the diagnosis, understand the drug list and notice the complications that belong to one disease and not the other.

What you need to know first

You need only everyday experience of a stiff or aching joint, and the ordinary idea that the immune system normally defends the body against infection. Every technical word — cartilage, synovium, autoimmune, disease-modifying drug — is defined below, so no previous rheumatology course is assumed.

Words to know (5)

Osteoarthritis: The most common form of arthritis, in which the protective cartilage that cushions the ends of the bones wears down over time, making the joint painful and stiff. A patient whose knee aches after a long walk and eases when he sits down may have osteoarthritis of the knee.
Rheumatoid arthritis: An autoimmune and inflammatory disease in which the immune system attacks healthy tissue in the joints, usually many joints at once and on both sides of the body. Swelling and tenderness in both wrists and both hands at the same time suggests rheumatoid arthritis rather than osteoarthritis.
Synovial membrane: The thin lining that covers the inside of the joint capsule and produces the lubricating fluid that lets the joint surfaces glide and nourishes the cartilage. In rheumatoid arthritis this lining becomes inflamed and thickened, and it is the tissue that damages the joint.
Autoimmune disease: A condition in which the immune system attacks the body’s own healthy cells by mistake instead of, or in addition to, defending it against infection. Rheumatoid arthritis is autoimmune, which is why it can inflame the heart, lungs and eyes as well as the joints.
Disease-modifying antirheumatic drug: A medicine that does not merely relieve pain but slows the disease process and protects joints and other tissues from permanent damage; it works best when started early. Clinical studies show that remission of rheumatoid arthritis is more likely when a disease-modifying drug is started early.

One idea at a timeIdea 1 / 5

In one sentence Arthritis is not one disease: osteoarthritis wears the joint surface away, while rheumatoid arthritis makes the immune system attack the joint lining.

Arthritis is not one disease: two different attacks on a joint

A joint is a meeting point between two bones, and the ends of those bones are covered by a smooth, slippery material called cartilage that lets the surfaces glide over each other. Around the joint runs a capsule lined by a thin membrane, the synovium, which makes a lubricating fluid. Arthritis means inflammation or damage in a joint, and the two commonest forms attack different parts of this structure. In osteoarthritis the cartilage itself wears away, so the problem is mechanical: the surfaces that should glide begin to grind, and the bone underneath and around the joint reacts. In rheumatoid arthritis the synovium is the target, and the damage is driven by the immune system rather than by load. Both diseases end in pain, swelling and deformity, but the cause decides which joints are hit, which other organs are at risk and which treatment can help.

For example

Two patients arrive with pain in one knee. One is a builder whose pain appears after a day of climbing ladders; the other has hot, swollen joints on both sides and feels feverish. The same word, arthritis, hides two different mechanisms.

Pause and check yourself

Which tissue fails first in osteoarthritis, and which tissue is attacked in rheumatoid arthritis?

Show the answer

In osteoarthritis the cartilage covering the bone ends wears away; in rheumatoid arthritis the immune system attacks the synovial lining of the joint.

Read detailed explanations

Osteoarthritis: a living tissue that can no longer keep repairing itself

Calling osteoarthritis simple wear and tear hides what is really happening in the tissue. Articular cartilage is avascular: it has no blood vessels of its own and is nourished by the synovial fluid that bathes it, which is one reason it repairs so poorly. It is maintained by scattered cells called chondrocytes, which build and renew a matrix of collagen fibres and water-binding proteoglycans. That matrix gives cartilage its resilience, squeezing fluid out under load and drawing it back when the load is removed. Osteoarthritis begins when this maintenance slips: enzymes released in the joint degrade the proteoglycans faster than the chondrocytes can replace them, the matrix loses water and stiffness, and the surface softens, fissures and eventually thins to bare bone. The joint space narrows on a radiograph.

The bone beneath, the subchondral plate, responds to the increased stress by thickening, a change called subchondral sclerosis, and small cysts and bony outgrowths called osteophytes form at the joint margins — the hard lumps a patient can feel through the skin. The capsule thickens and the synovium may become mildly inflamed, producing the mild swelling that accompanies it; marked redness or heat points instead to inflammatory or infective arthritis. Mechanical load is central: the force transmitted across the knee when climbing stairs or squatting is several times body weight, so obesity, malalignment such as a bow-legged stance, previous meniscal surgery and ligament injury all concentrate stress on one region of the surface.

Haemochromatosis, in which excess iron is deposited in tissues, damages cartilage directly, and diabetes and a genetic predisposition add to the risk. This also explains why the greater frequency in women is not accounted for by oestrogen alone: biomechanics, muscle strength and hormonal change after the menopause all contribute. The treatment list follows the mechanism.

Unloading the joint through weight reduction, walking aids, insoles and orthotics lowers the stress; strengthening the quadriceps stabilises the knee; paracetamol and NSAIDs control pain, although NSAIDs carry gastrointestinal, renal and bleeding risks that matter in older patients; duloxetine addresses the chronic pain component; an intra-articular corticosteroid gives short-term relief and is limited because repeated injection may accelerate damage; hyaluronic acid injections lubricate for a time; osteotomy redistributes load in single-compartment disease; and total arthroplasty replaces the surface when pain and disability become intolerable. The nurse looking after such a patient watches analgesia intake, bowel and kidney function, bleeding risk when anticoagulants are given, and the risk of falls when a painful limb is unloaded.

Rheumatoid arthritis: a systemic autoimmune disease, not only a joint disease

The joint damage of rheumatoid arthritis begins in the synovium, but the process that drives it is systemic, and that is why the disease can shorten life as well as deform hands. The inflamed synovium thickens and grows a sheet of invasive tissue called pannus, which releases cytokines such as tumour necrosis factor and interleukin-6. These signalling molecules recruit more immune cells, activate osteoclasts and digest the collagen and mineral of cartilage and bone, producing the marginal erosions seen on imaging. Because the same cytokines circulate in the blood, the inflammation is not confined to the joint.

The most important consequence is cardiovascular: chronic inflammation accelerates atherosclerosis, and heart disease is a leading cause of premature death in rheumatoid arthritis, so blood pressure, blood lipids and smoking cessation belong to rheumatology care. The lungs may develop interstitial lung disease or a pleural effusion; the eyes may become dry in sicca syndrome or painfully inflamed in scleritis and episcleritis; the skin may show rheumatoid nodules; and peripheral nerves may be damaged by vasculitis or compression. Chronic inflammation also lowers haemoglobin, producing anaemia of chronic disease, and the combination of inflammation and corticosteroid therapy accelerates osteoporosis.

A less obvious but dangerous site is the neck: inflammation of the atlantoaxial joint can allow the first vertebra to slide on the second, so the spinal cord is at risk during intubation or a sudden neck movement, and the anaesthetist and nurse must immobilise the neck in line rather than force it. Diagnosis rests on the pattern plus laboratory support. Rheumatoid factor is present in many patients but is not specific; anti-cyclic citrullinated peptide antibodies are more specific and predict more aggressive disease; the erythrocyte sedimentation rate and C-reactive protein measure the degree of inflammation, and ultrasound or MRI can show erosion before a radiograph does.

The genetic contribution is carried largely by HLA-DRB1, and cigarette smoking is the strongest environmental risk factor, probably because it encourages citrullination of proteins in the lung and gums, which triggers the immune response in a susceptible person. Treatment follows a treat-to-target strategy: methotrexate is usually the first disease-modifying drug, given with folic acid and monitored by liver enzymes and blood counts; leflunomide, hydroxychloroquine and sulfasalazine are alternatives; biologics such as etanercept, adalimumab, infliximab, tocilizumab, abatacept and rituximab block specific cytokine pathways; Janus kinase inhibitors such as tofacitinib are taken by mouth, but higher doses increase the risk of clots, serious cardiac events and cancer.

Because these drugs suppress immunity, the nurse checks for infection, ensures screening for tuberculosis and hepatitis and appropriate vaccination before treatment, and takes a new fever, cough or weight loss seriously.

Arthritis in a child is a different problem: juvenile idiopathic arthritis

Arthritis in a child is not the adult disease in a smaller body. Juvenile idiopathic arthritis, once called juvenile rheumatoid arthritis, is defined as joint inflammation and stiffness lasting more than six weeks in a child aged sixteen or younger, and it affects roughly fifty thousand children in the United States. It is grouped by how many joints are involved and by which other tissues are affected. Oligoarticular disease, the commonest form at about half of cases, involves four or fewer joints and often only one, usually a knee or an ankle, and it is more frequent in girls under eight. Polyarticular disease, about a third of cases, affects five or more joints, large and small, on both sides; children who carry IgM rheumatoid factor tend to have a more severe course resembling adult rheumatoid arthritis.

Psoriatic arthritis combines joint disease with psoriasis or a family history of it, and it may bring nail changes and dactylitis, a diffuse swelling of a finger or toe. Enthesitis-related arthritis inflames the entheses, the points where tendons and ligaments attach to bone, and it may involve the spine; it is commonest in boys over six. Systemic disease, about a fifth of cases, causes a high spiking fever — a daily fever of at least 102 degrees, which is 102 degrees Fahrenheit, about 39 degrees Celsius, for two weeks or longer — together with a rash and inflammation of internal organs, and it can be complicated by macrophage activation syndrome, a severe multi-organ reaction that can be fatal. Two complications shape nursing care.

Eye inflammation, or uveitis, is often silent, so every child needs regular examination with a slit lamp; left untreated it can cause cataracts, glaucoma and blindness. Growth can be disturbed both by the disease and by corticosteroid treatment, so growth is plotted and steroids are used for the shortest possible time. Blood tests may show a raised erythrocyte sedimentation rate or C-reactive protein, and antinuclear antibodies mark an increased chance of eye disease, while rheumatoid factor and anti-cyclic citrullinated peptide antibodies identify children at higher risk of joint damage; in many children, however, all these tests are normal, so imaging is used mainly to exclude a fracture, a tumour, an infection or a congenital defect.

Treatment aims to relieve pain, preserve function and prevent joint destruction: NSAIDs for symptoms, methotrexate as the first disease-modifying drug, tumour necrosis factor blockers and other biologics when needed, corticosteroids sparingly, physiotherapy and splints to keep joints in a good position, and surgery only in severe cases. Two categories must stay separate — oligoarticular means four or fewer joints, while monoarticular means a single joint — and the older text prints MIR where MRI is meant; the modern name is juvenile idiopathic arthritis.

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Two arthritides, two tissues under attack

The same joint, drawn twice. On the left, osteoarthritis: the smooth cartilage that should let the bone ends glide is worn through in the middle, the bone underneath thickens and a bony outgrowth forms at the margin. On the right, rheumatoid arthritis: the synovial lining is inflamed and thickened into an invasive sheet that erodes cartilage and bone from both edges. The strip below lists the bedside clues that separate the two.

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01 / 4Osteoarthritis: cartilage worn through

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Osteoarthritis: cartilage worn through

In osteoarthritis the smooth cartilage covering the bone ends thins and breaks down, so the surfaces that should glide begin to grind. Cartilage has almost no blood supply of its own and repairs poorly, which is why the loss is permanent and why the joint space narrows on an X-ray. The bone beneath and around the joint thickens in response to the extra load, and pain is worst when the joint is used and eases with rest.

Schematic, not anatomical: the two drawings are the same joint shown twice, not two different joints. The cartilage is drawn as a band with a gap where it is worn through, the osteophyte as a single lump at one margin, and the pannus as two shaded areas; a real joint has these changes in three dimensions and in several places at once.

Key points to remember

Osteoarthritis is the commonest arthritis: the protective cartilage at the bone ends wears away, so pain is worse with use and eases with rest, and the knees, hips, hands and spine are most often affected.
Rheumatoid arthritis is an autoimmune, inflammatory and systemic disease: the synovial lining is attacked, many joints are involved symmetrically, and the heart, lungs, eyes, nerves and skin may also be affected.
The pattern separates them: osteoarthritis pain follows use and the patient feels otherwise well, while rheumatoid arthritis brings morning stiffness lasting more than an hour, symmetrical swelling, fatigue, fever and weight loss.
Treatment follows the cause: osteoarthritis is managed with pain relief and load reduction, with steroid injections limited to about three or four a year, while rheumatoid arthritis needs early disease-modifying drugs to protect joints and organs.
A joint that is hot, swollen and stiff in the morning is not simple wear: it needs prompt assessment, because early treatment changes the outcome in inflammatory arthritis.

Go deeper

Worked example

Two patients with painful hands: separating the two arthritides. During one clinic session you meet two women with painful hands. Mrs A is 61 and reports that the base of both thumbs and the end joints of her fingers ache after she has been knitting or gardening, that her hands feel stiff for a few minutes when she stops, and that she has no other complaints. Mrs B is 44 and reports eight weeks of swelling in both wrists and the knuckles of both hands, stiffness that takes about ninety minutes to wear off each morning, fatigue, and a loss of appetite with some weight loss. Use the structure and the pattern to work out what is happening in each pair of hands.

Name the tissues at risk. Each joint has cartilage covering the bone ends and a synovial lining making lubricating fluid. Deciding which of these two tissues is under attack is the first step, because osteoarthritis is a failure of cartilage under load while rheumatoid arthritis is an immune attack on the synovium.
Read the timing of the pain. Mrs A’s pain appears after activity and settles within minutes of resting, which is the mechanical pattern of osteoarthritis. Mrs B’s stiffness is worst after a night of rest and lasts about ninety minutes, which is the inflammatory pattern of rheumatoid arthritis; pain that improves with movement rather than with rest is a strong clue.
Read the distribution. Mrs A’s pain sits in the thumb base and the end joints of the fingers, and it is not symmetrical in a striking way; those are typical sites of osteoarthritis. Mrs B has both wrists and the knuckles of both hands involved at the same time, a symmetrical pattern in the small joints that points to rheumatoid arthritis rather than to wear.
Look for general symptoms. Mrs A feels well apart from her hands, which fits a mechanical disease limited to the joints. Mrs B has fatigue, loss of appetite and weight loss, which tell you the process is systemic: the same inflammation that swells her joints can also affect her heart, lungs, eyes and skin, and it needs to be assessed rather than treated as simple arthritis.
Turn the pattern into a plan. Mrs A needs pain relief, load reduction, physiotherapy and occupational therapy, with joint replacement kept for later if function deteriorates. Mrs B needs urgent referral for inflammatory arthritis, because early disease-modifying treatment makes remission more likely and protects her joints and organs. Her nurse will also check for infection before and during immunosuppressive treatment and will watch for extra-articular problems.

The same word — arthritis — describes the two patients, but the tissue that is failing is different, and that difference produces every clue you collected: the timing of the pain, the symmetry, the joints involved and the presence or absence of general illness. Osteoarthritis is managed by reducing pain and load; rheumatoid arthritis is a systemic autoimmune disease that must be treated early with disease-modifying drugs, and it requires the nurse to think beyond the joints.

Common misconception

Many beginners believe that rheumatoid arthritis is simply a more advanced osteoarthritis — the same worn joint, further along — and that all arthritis will eventually need the same painkillers. The two are different diseases with different tissues under attack. Osteoarthritis is mechanical: cartilage wears away in joints that take load, and the patient is otherwise well. Rheumatoid arthritis is autoimmune and systemic: the immune system inflames the joint lining, many joints are affected symmetrically, and the heart, lungs, eyes, nerves and skin can be involved. That is why one is managed with pain relief and load reduction while the other needs early disease-modifying drugs and monitoring for infection and organ damage.

Check your reasoning

A patient tells you that both of her knees hurt when she climbs the stairs, but that they feel better once she sits down, and that she is otherwise well. Which questions would you ask to be sure this is osteoarthritis and not an inflammatory arthritis?

Reveal an answer

Ask first about the morning: how long does the stiffness last after waking? A few minutes fits osteoarthritis, while more than an hour fits an inflammatory arthritis. Ask next about symmetry and how many joints are involved: one or two load-bearing joints suggest osteoarthritis, whereas several small joints on both sides at once suggest rheumatoid arthritis. Ask about general symptoms — fatigue, fever, weight loss, eye redness or breathlessness — because these point to a systemic disease. Finally, ask about swelling, warmth and tenderness, since inflammatory joints are swollen and warm, and remember that on examination a grating, creaking joint with hard bony lumps and little swelling is the mechanical picture, while a soft, boggy, warm joint suggests inflammation.

Where this comes from

MUSCULOSKELETAL SYSTEM PATHOLOGIES lecture notes (supplied), Level 200 nursing · Lines 645–753 under “JOINT DISORDER”: osteoarthritis as the most common arthritis with cartilage wear, the risk factors (age, female sex, joint injury, repeated stress, obesity, genetics, bone deformity, metabolic disease), the signs and symptoms (pain, stiffness, swelling, tenderness, loss of flexibility, grating sensation, bone spurs), diagnosis (physical examination, X-ray, MRI, blood tests, joint fluid analysis) and management (acetaminophen, NSAIDs, duloxetine, physical and occupational therapy, TENS, cortisone injections limited to three or four a year, hyaluronic acid, osteotomy, joint replacement); rheumatoid arthritis as an autoimmune and inflammatory disease with inflamed joint lining, symmetrical symptoms, general features (weight loss, fever, fatigue, weakness) and involvement of heart, lungs, nerves, eyes and skin, its risk factors (sex, age about 50, family history, smoking, excess weight), diagnosis and treatment (NSAIDs, steroids, conventional and biologic DMARDs, targeted synthetic DMARDs, synovectomy, tendon repair, joint fusion, total joint replacement); and juvenile arthritis with its types, complications, blood tests and treatments.
Beyond the supplied notes: standard rheumatology and immunology · the avascular nature of articular cartilage and its nutrition from synovial fluid, chondrocytes, collagen and proteoglycans, subchondral sclerosis, osteophytes and the joint-load multiples of stair climbing and squatting; the pannus, tumour necrosis factor and interleukin-6, marginal erosions, accelerated atherosclerosis and cardiovascular death, interstitial lung disease and pleural effusion, sicca syndrome, scleritis and episcleritis, rheumatoid nodules, vasculitis, anaemia of chronic disease, atlantoaxial subluxation and airway management, rheumatoid factor, anti-cyclic citrullinated peptide antibodies, HLA-DRB1, smoking and citrullination, treat-to-target methotrexate with folic acid and blood monitoring, TNF blockers and Janus kinase inhibitors; and paediatric uveitis screening by slit lamp, macrophage activation syndrome, and the growth effects of the disease and of corticosteroids. The supplied notes list the drugs, tests and complications but do not explain the mechanisms, which are uncontroversial standard content.
Corrections to the supplied notes · Corrections to the supplied notes, labelled as such: the notes print “MIR” for magnetic resonance imaging, written MRI in this section; the systemic juvenile arthritis fever is given without units as “at least 102°”, and is 102 degrees Fahrenheit, about 39 degrees Celsius; the notes merge oligoarticular disease (four or fewer joints) with monoarticular disease (a single joint) and give both as about half of children, so the two categories are kept separate here; the notes attribute the female preponderance in osteoarthritis to “hormones like estrogen”, which is an oversimplification, since biomechanics, muscle strength and post-menopausal hormonal change all contribute; and the older term “juvenile rheumatoid arthritis” is now juvenile idiopathic arthritis. These are standard reference facts used to correct, not to extend, the supplied notes.

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About this course and its sources

The musculoskeletal and neurological lessons build on the supplied Level 200 nursing notes. Reproductive, respiratory, skin and nursing-response lessons use cited external references. Diagrams are original educational schematics. Sections that go beyond the supplied notes say so in their sources. Specialist clinical and French-language editorial review remain pending.