Rheumatoid arthritis and osteoarthritis: Pathology review

Definitions & Key takeaways

Rheumatoid arthritis (RA) and osteoarthritis (OA) are both types of arthritis, but they have different causes and characteristics.

Rheumatoid arthritis is an autoimmune inflammatory disease that causes progressive and symmetric destruction of at least three joints, especially the proximal interphalangeal joints, which leads to morning stiffness that lasts for more than an hour and improves with use. It can also present with extra-articular symptoms like uveitis, pulmonary fibrosis, and rheumatoid nodules. The treatment of rheumatoid arthritis involves non-biological and biological DMARDs, nonsteroidal anti-inflammatory drugs (NSAIDs), and glucocorticoids.

Osteoarthritis, on the other hand, is a chronic condition characterized by the breakdown of joint cartilage and underlying bone followed by inadequate repair. Now, unlike rheumatoid arthritis, which is an autoimmune disorder, osteoarthritis is considered a mechanical degenerative joint disorder. This is because the main culprit seems to be the daily stress applied to joints in our lifetime, especially to weight-bearing joints like those of the ankle, knee, and hip. Symptoms of OA include joint pain, stiffness, and decreased range of motion. Treatment of OA involves losing weight, physical therapy, and pain management with drugs like acetaminophen and NSAIDs.

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Case Study0:00–1:11

Jody is a 55 year old woman who presents with a 6 month history of bilateral hand and wrist stiffness. She mentions that the stiffness lasts for more than an hour a day but tends to improve as she uses the affected joints.
Examination shows swelling, limited range of movement, and subcutaneous nodules over the proximal interphalangeal joints, but no redness.
Then you see Kerry, a 60 year old woman who comes in with a 1 year history of pain in the right knee that has gotten progressively worse.
The pain is worse in the evening or with use of the affected limb and is associated with stiffness, which typically occurs at rest and lasts around 10 to 15 minutes.
Examination reveals Kerry is obese, has bowing of the right knee, and that the affected joint has a limited range of motion.
Blood tests are ordered in both cases, showing in Jody's case high levels of rheumatoid factor (RF) and anti-citrullinated peptide antibody (ACPA), whereas in Kerry's case both antibodies were absent.Both people have arthritis.
Now, a healthy joint usually consists of two bones, each with its own layer of articular cartilage. Articular cartilage is a type of connective tissue with a lubricated surface that acts like a protective cushion for bones to smoothly glide against.

Physiology1:11–2:08

Now, there are many types of joints, including fibrous, cartilaginous, and synovial joints, which have additional components depending on their function.
For example, synovial joints, like those of the wrist, elbow, knees, shoulders, and hips, are mobile joints that connect two bones via a fibrous capsule that is continuous with the periosteum, which is the outer layer of bones.
The fibrous capsule is lined with a synovial membrane that has cells that remove debris and produce synovial fluid, which is a viscous fluid found inside the joint capsule to lubricate the joint.
Together, the synovial membrane and articular cartilage form the inner lining of the joint space. Now, arthritis refers to a group of diseases that cause destruction of one or more joints, and it can be classified as inflammatory or non-inflammatory.

Pathology2:08–3:30

Inflammatory arthritis is caused by an )immune response attacking the joints. It includes conditions with unknown cause, like rheumatoid arthritis and juvenile idiopathic arthritis, or it can be secondary to diseases like systemic lupus erythematosus and Sjogren syndrome.
On the other hand, non-inflammatory arthritis is caused by mechanical wear and tear, and it is mostly represented by osteoarthritis.
Generally, in terms of symptoms, there are a few differences between inflammatory and non-inflammatory arthritis. Ok so inflammatory conditions are usually accompanied by joint swelling, erythema, prolonged morning stiffness lasting more than one hour, and symmetric pain that improves with use.
Most of these conditions are also associated with extra-articular symptoms, like fever and fatigue. On the other hand, non-inflammatory arthritis is usually suggested by asymmetric pain that gets worse with use and affects weight bearing joints, like the knee and the hip, and morning stiffness that lasts less than one hour.
Extra-articular symptoms are usually absent in non-inflammatory arthritis. Let's begin with the most common type of inflammatory arthritis.

Rheumatoid Arthritis 3:30–14:20

Rheumatoid arthritis is a chronic, progressive, and inflammatory disorder that affects synovial joints and, sometimes, other parts of the body like the skin and the lungs.
It is thought to be an autoimmune reaction, however, the exact cause is unknown. Generally speaking, it seems to be associated with environmental risk factors like infections and smoking, and with a genetic predisposition, like in biologically female individuals, and having the alleles HLA-DR1 and HLA–DR4.
So basically, it is believed that environmental risk factors in those with genetic predisposition end up modifying normal articular proteins in synovial joints.
As a consequence, the modified proteins end up confusing the cells of our immune system, which fail to recognize them as being self, or part of the normal human body, so at this point this protein is now a self antigen.
Antigen presenting cells then pick up the self antigen and take them to the lymph nodes, where they activate CD4+ T helper cells.
T helper cells then stimulate the nearby B cells to proliferate and differentiate into plasma cells, which produce specific autoantibodies against these self antigens, namely rheumatoid factor or RF, and anti-cyclic citrullinated peptide antibody or anti-CCP.
Soon after, both T helper cells and antibodies enter the circulation and reach the joints. Once there, T cells secrete cytokines to recruit more inflammatory cells like macrophages into the joint space.
Macrophages will also produce inflammatory cytokines, like tumor necrosis factor, or TNF-α, interleukin- 1 or IL-1, and interleukin- 6, IL-6, which, together with the cytokines released by T cells, stimulate synovial cells to proliferate.
This increase in synovial cells and immune cells in the joint creates a pannus, which is a thick, swollen synovial membrane with granulation or scar tissue, made up of fibroblasts, myofibroblasts, and inflammatory cells.
Over time, the cytokines released in the pannus start to break down the articular cartilage, so the underlying bones are exposed and can directly rub against one another, leading to bone erosion.
Meanwhile, the antibodies that enter the joint space bind to their targets and form immune complexes that accumulate in the synovial fluid, activating the complement system, which further contributes to joint inflammation and injury.
Now, when it comes to articular symptoms, rheumatoid arthritis typically involves three or more joints symmetrically, meaning the same joint groups on both sides of the body, like the finger joints in both hands for instance.
The hallmark symptom of rheumatoid arthritis is chronic morning stiffness that lasts for over an hour, improves with use, and has lasted for more than 6 weeks.
The most frequent sites are the proximal interphalangeal joints of the hand, the metacarpo-phalangeal joints of the hand, and the wrists.
By contrast, the first carpometacarpal joint and the distal interphalangeal joints are rarely involved because they contain very little synovium.
Associated symptoms include reduced grip strength and range of motion, pain, and swelling. As a particularity, swelling in rheumatoid arthritis is different from the one in osteoarthritis.
In rheumatoid arthritis, the swelling is caused by soft tissue edema secondary to inflammation, whereas in osteoarthritis swelling is secondary to bony overgrowth that makes the joint look larger.
Another distinction to help you out is that rheumatoid arthritis doesn't usually cause redness or warmth because the inflammatory process is so gradual and chronic.
However, sometimes it can present with acute inflammatory signs such as edema, redness, warmth, and pain when there's an acute episode of rheumatoid arthritis, also called a flare.Now, other joints of the body besides the hands can be affected.
For example, in the feet, it's usually the metatarsophalangeal joints, causing the individual to bear more weight on the heels and hyperextend their toes.
Hip involvement usually happens later in the disease, causing pain in the groin, thigh, or low back. One very dangerous spot is the C1-C2 joint, or the atlantoaxial joint, which is the only synovial joint in the spine.
When it's affected, it can cause neck pain, and sometimes extension of the neck during endotracheal intubation can worsen the subluxation, leading to acute compression of the spinal cord or vertebral arteries.
This can lead to spinal cord compression and tetraplegia, which is paralysis of all four limbs and torso.As the disease progresses, there are also a series of deformities that can occur due to joint destruction.
One of them is swan-neck deformity, which doesn't occur in the neck but in the fingers, causing them to deform and resemble the shape of a swan's neck.
Specifically, the distal interphalangeal joint of the affected finger is in flexion or bent, while the proximal interphalangeal joint is in hyperextension or bent beyond its normal range of motion.
There's also the Boutonniere deformity, where roles reverse, meaning the proximal interphalangeal joint flexes to face the palm, and the distal interphalangeal joint is in hyperextension facing away from the palm.
Sometimes, when the metacarpophalangeal joints are severely affected, an ulnar drift can occur, where the fingers lean away from the thumb and toward the pinky.
This is due to the weakened radiocarpal ligaments that cause radial rotation of the metacarpals and carpus on the radius, which results in ulnar deviation of the joint.
Another important deformity is the Z-deformity, where the thumb flexes at the metacarpophalangeal joint and hyperextends at the interphalangeal joint.
This makes the finger look as if the individual is trying to hitch a ride, which is why it is also called the hitchhiker thumb deformity.
Now, if the spine is involved, cervical joint destruction can lead to vertebral misalignment or subluxation, causing pain, neurologic deficits, and deformity.
Finally, there can also be toe deformities like the claw toe deformity, where the metatarsophalangeal joint is hyperextended, while the proximal and distal interphalangeal joints are flexed.
This makes affected toes to look like bird claws. Unfortunately, the cytokines released by the immune system don't stay in just one place.
Instead, they can reach multiple organ systems, causing extra-articular symptoms. For example, interleukin- 1 and 6 travel to the brain, where they act as pyrogens, inducing fever, fatigue, loss of appetite and, ultimately, weight loss.
They can also lead to inflammation of the uvea, which is the layer of tissue beneath the white of the eye or sclera, causing uveitis.
Some signs of uveitis include eye pain, conjunctival redness, blurry vision, miosis, and rarely with hypopyon or accumulation of pus in the anterior chamber of the eye.
If the sclera is involved, it can cause scleritis. Now, in the skin, as well as in many visceral organs, the inflammatory cytokines lead to the formation of rheumatoid nodules, which are bumps with a central area of fibrinoid necrosis that's surrounded by palisading histiocytes, a type of macrophage.
Palisading means the cells are arranged in layers around the necrotic area, parallel with each other, almost like a picket fence.
On examination, these are seen as singular or multiple subcutaneous nodules that are firm to the touch, non painful, and distributed around the affected joint.
In the soft tissue, the disease can lead to carpal tunnel syndrome. The carpal tunnel is a narrow passageway formed by the carpal bones and the transverse carpal ligament at the wrist, which gives passage to the median nerve and muscle tendons.
Because rheumatoid arthritis causes tendon inflammation, these swell up and compress the median nerve, causing carpal tunnel syndrome and symptoms such as paresthesia or tingling sensation, pain, and numbness of the hand.Blood vessels can also be affected, causing wall inflammation resulting and in various forms of vasculitis, which can make blood vessels more prone to developing atheromatous or fibrofatty plaques.
These can lead to cardiovascular disease like myocardial infarction and stroke. In fact, cardiovascular disease is the primary cause of mortality associated with rheumatoid arthritis.
Meanwhile, within the lung interstitium, fibroblasts get activated and proliferate, causing pulmonary fibrosis that impairs the alveolar gas exchange.
The pleural cavities surrounding the lungs can get inflamed as well, causing them to fill up with fluid, which is known as pleural effusion, and it can impair lung expansion too, interfering even more with gas exchange.
Additionally, there's Caplan's syndrome, which is when the individual has both pneumoconiosis and rheumatoid arthritis, and this tends to manifest as intrapulmonary nodules.
The liver can start producing high amounts of hepcidin in response to inflammatory cytokines. Hepcidin decreases serum iron levels by inhibiting its absorption by the gut and trapping it into macrophages or liver cells, leading to anemia of chronic disease.
In the spleen, rheumatoid arthritis can lead to splenomegaly and neutropenia, a combination called Felty syndrome. It can also be associated with Sjogren syndrome, which is an autoimmune disease that primarily attacks the lacrimal and salivary glands, impairing their ability to secrete their fluids and resulting in dry eyes, mouth, and skin among many other symptoms.
And finally, rheumatoid arthritis can lead to AA amyloidosis, which is a type of amyloidosis that occurs as a reaction to another illness.
In short, rheumatoid arthritis causes the liver to produce a protein called SAA or serum amyloid A protein in high levels, which is a normal reaction.
However, if inflammation persists, a small portion of the SAA protein, called AA protein, will separate from SAA and deposit in organs as AA amyloid, especially in the kidneys, where it causes organ damage.
Diagnosis of rheumatoid arthritis is based on a complete clinical evaluation, followed by a series of tests, since some conditions like Parvovirus B19 infection may mimic the symptoms of rheumatoid arthritis.

Rheumatoid Ar. Diagnosis14:20–17:17

Okay, so when it comes to blood tests, there might be signs of anemia, thrombocytosis, mild leukocytosis, and elevated erythrocyte sedimentation rate or ESR and C-reactive protein or CRP, all of which are caused by the chronic inflammation associated with the disease.
It's also important to test for autoantibodies like RF and anti-CCP.For your exam, you should remember that rheumatoid factor is an IgM antibody that targets the constant Fc component of human IgG antibodies.
Anti-cyclic citrullinated peptide antibody is an antibody that targets citrullinated proteins, which are proteins whose arginine residues have been chemically modified to citrulline through a process called citrullination.
A high-yield fact you should know is that although RF is associated with rheumatoid arthritis, it is not highly specific, as it is positive in just 70% of cases.
In addition, RF can also be elevated in other diseases like Sjögren syndrome, lupus, sarcoidosis, and hepatitis B, among many others.
On the other hand, anti-CCP is more specific of rheumatoid arthritis, as it has a specificity of almost 96%. This means that there are cases of rheumatoid arthritis with negative serology.
In these cases, diagnosis is based solely on clinical findings and imaging. A minority of individuals could also present antinuclear antibodies or ANA, which are formed against the normal proteins of a cell's nucleus.Radiographs of the affected joint are also important for diagnosis.
Over time, some possible changes might include juxta-articular osteopenia, or decreased bone density around affected joints that shows as areas with increased transparency on an x-ray; soft tissue swelling, which is seen as a thick halo around the bone; narrowing of the joint space; bone erosions, which look like someone bit into the bone; and rarely, subchondral cysts, which are sacs of hyaluronic acid that form in the subchondral bone, the layer of bone just under the cartilage.
On an x-ray, subchondral cysts look like dark, round, and fairly well delimited areas inside the bone.In some cases, arthrocentesis can be done, where synovial fluid is collected from an affected joint and examined under a microscope and sent for Gram stain and cultures, especially during a flare, to make sure there's no evidence of crystals like in gout or pseudogout, or signs of infection like in septic arthritis.There's no cure for rheumatoid arthritis, but there are ways to keep the disease under control.

Rheumatoid Ar. Treatment17:17–22:24

The main treatment consists of long term medications called disease modifying antirheumatic drugs or DMARDs, which can be non-biological or biological.
Most individuals with an acute rheumatoid arthritis flare are started on non-biological DMARDs, like methotrexate, leflunomide, hydroxychloroquine, and sulfasalazine.
The most common monotherapy is methotrexate, which is a folic acid analog that inhibits dihydrofolate reductase, an enzyme that participates in the tetrahydrofolate synthesis, which in return inhibits the synthesis of DNA, RNA, and proteins.
However, in rheumatoid arthritis, this doesn't seem to be the main mechanism by which methotrexate works. Instead, there seem to be multiple other mechanisms involved, including immune system inhibition.
Some notable side effects include pulmonary fibrosis, hepatotoxicity, stomatitis or painful mouth ulcers, and nephrotoxicity.
Now, methotrexate can also lead to folate deficiency, which can cause megaloblastic anemia, a macrocytic type of anemia that results from inhibition of DNA synthesis during red blood cell production.
Another common side effect is myelosuppression, which is reversible with leucovorin rescue. This is because leucovorin, also called folinic acid, has vitamin activity equivalent to that of folic acid, but doesn't require dihydrofolate reductase to be metabolised.
And finally, methotrexate is teratogenic, causing neural tube defects via folic acid deficiency, which means it should not be used by pregnant women.
When Methotrexate monotherapy doesn't work or it's contraindicated, the person should take another DMARD. There's leflunomide, which reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis, which suppresses T cell proliferation.
Some side effects include diarrhea, hypertension, hepatotoxicity, and teratogenicity. Then there's hydroxychloroquine, which is generally considered to be the safest DMARD, and a “go to” drug for pregnancy.
It works by inhibiting the cells of the immune system through multiple mechanisms, such as increasing lysosomal pH in antigen-presenting cells, and blocking toll-like receptors on plasmacytoid dendritic cells.
Toll-like receptors are surface proteins that have a role in recognising the pathogens that enter our bodies. The most important side effects are eye toxicity, hepatotoxicity, excessive coloring of the skin, nausea, and diarrhea.
And finally, sulfasalazine is a combination of sulfapyridine, an antibiotic, and 5-aminosalicylic acid, an anti-inflammatory drug, and it is activated by colonic bacteria.
Side effects include malaise, nausea, sulfonamide toxicity, and reversible oligospermia.In case of severe disease resistant to combination therapy, individuals should be started on biological DMARDs, also called biologics, which suppress some part of the immune system.
For example, abatacept suppresses T cells, rituximab suppresses B cells, while others block specific cytokines. One of the medications that block cytokines activity is etanercept.It reduces TNF-alpha activity by acting as a decoy receptor, preventing the cytokine from attaching to its receptors on healthy tissues.
There's also infliximab and adalimumab, two anti-TNF-alpha monoclonal antibodies against the cytokine. Now, a major downside of these drugs that you might come across in your test is the fact that they increase predisposition to infection, including reactivation of latent tuberculosis, since TNF is important in granuloma formation and stabilization.
Hence, keep in mind that you always have to test for latent TB before starting TNF-alpha inhibitors. They can also lead to drug-induced lupus.
Now, to help you differentiate between the two, pharmaceutical companies use the cept suffix to indicate the medication is a protein receptor and the mab suffix to indicate it's a monoclonal antibody.In addition, something that's frequently tested is that there are also short term medications used to provide analgesia and symptom relief.
These consist of nonsteroidal anti-inflammatory drugs or NSAIDs like naproxen, or glucocorticoids like prednisone, which are used especially during flares because they are fast acting and provide quicker symptom relief when compared to DMARDs.
NSAIDs are preferred over glucocorticoids because they have fewer side effects. Next, there's a family of inflammatory arthritides called juvenile idiopathic arthritis that occur in young individuals under the age of 16.

Juvenile Idiopathic Art.22:24–24:14

The cause is unknown, hence the name idiopathic, but it can be associated with the gene HLA-B21 and with triggers such as infections.
It is also thought to have an autoimmune basis, which leads to the recruitment and activation of inflammatory cells that release proinflammatory cytokines.
These cytokines reach different parts of the body and cause inflammation and tissue injury, leading to the main symptoms of juvenile idiopathic arthritis.
Typically, there's symmetrical involvement of larger joints, like the knee or the ankle. These individuals usually present with the typical inflammatory joint signs, which are worse in the morning or with rest.
The most common type is called oligoarticular arthritis, in which there are up to 4 joints affected. Then there's polyarticular arthritis, which affects 5 or more joints.
These two types can also be associated with uveitis, and if tendons are involved, enthesitis might develop. Finally, there's another type called systemic juvenile idiopathic arthritis, which is rather frequently tested on exams; it affects not only the joints but the whole body.
The skin can be affected too, mainly showing a salmon pink macular rash that often appears with fever. Other systemic abnormalities that can occur include daily spiking fever, splenomegaly, generalized adenopathy, and pericarditis or pleuritis.
Something else worth noting is that joint involvement can actually occur weeks or months after systemic symptoms, making diagnosis difficult.
Diagnosis is mostly clinical, but it can also include blood tests, where typical findings include leukocytosis, thrombocytosis, anemia, and increased levels of ESR and CRP, while RF, ANA, and anti-CCP can be positive or negative.

JIA Diagnosis24:14–24:36

Genetic testing might be positive for HLA-B21.Treatment involves intra-articular corticosteroid injections, NSAIDs, and DMARDs, particularly methotrexate and biologic agents.

JIA Treatment24:36–24:52

If methotrexate is not effective, TNF inhibitors are used.All right, let's move on to non-inflammatory arthritis, which usually refers to osteoarthritis.

Osteoarthritis24:52–29:45

In fact, it is the most common type of arthritis overall. Okay, so osteoarthritis is a chronic condition characterized by the breakdown of joint cartilage and underlying bone followed by inadequate repair.
Now, unlike rheumatoid arthritis, which is an autoimmune disorder, osteoarthritis is considered a mechanical degenerative joint disorder.
This is because the main culprit seems to be the daily stress applied to joints in our lifetime, especially to weight-bearing joints like those of the ankle, knee, and hip.
This is why the biggest risk factor for osteoarthritis is age, alongside joint injury, obesity, and altered walking patterns, which can increase joint stress.
Now, although osteoarthritis is traditionally considered a non-inflammatory disease, recent data suggest that inflammation seems to be involved in osteoarthritis as well, especially proinflammatory cytokines like IL-1, IL-6, and TNF-alpha that can break down cartilage through proteolysis or by blocking the formation of new cartilage.Now, regardless of the initial cause of damage, chondrocytes in the joint can repair the cartilage by producing cartilaginous matrix made up of glycosaminoglycans, proteoglycans, collagen fibers, and sometimes elastin.
In early osteoarthritis, chondrocytes produce high levels of proteoglycans, which are glycosylated proteins, and type II collagen.
At some point, however, something causes them to switch over to making a different type of collagen, which is type I collagen.
Unfortunately, type I collagen doesn't interact with the proteoglycans in the same way as type II does, leading to an overall decrease in elasticity in the cartilage matrix, allowing it to break down.
This stage usually takes years to develop.Eventually, because chondrocytes aren't able to keep up with chronic damage, they undergo apoptosis, or programmed cell death.
As a result, the cartilage gets softer, weaker, and continues to lose elasticity, and it even starts to flake off into the synovial space as fragments called joint mice.
This activates the type A cells of the synovium, whose purpose is to remove synovial debris, as well as immune cells like lymphocytes and macrophages, which release proinflammatory cytokines that cause inflammation of the synovium or synovitis.
As the destructive process progresses, fibrillations form, which are essentially cracks or clefts on what used to be a smooth articular surface.
If no treatment is provided, the cartilage will continue to erode away until the bones are exposed, allowing them to rub with one another, which causes bone eburnation, making it look like polished ivory.
Now, the subchondral bone reacts to the articular damage by causing a hypertrophic reaction that leads to new bone formation at the joint margins called osteophytes, which makes the joints look wider.
The traumatized subchondral bone may also develop subchondral cysts, which are attributable either to osseous necrosis secondary to chronic erosion or to the intrusion of synovial fluid.Symptoms of osteoarthritis are high-yield.
The condition usually involves less than four joints asymmetrically. Regarding its location, injury typically occurs in weight-bearing joints like the knee, hip, or ankle.
In the hand, unlike rheumatoid arthritis, it most often affects the distal interphalangeal joints, but the proximal interphalangeal joints can be affected as well.
However, metacarpophalangeal joints are rarely affected. Individuals often experience joint pain that tends to worsen with activity and is much more pronounced in the evening.
Additionally, there can also be joint stiffening, which lasts less than 30 minutes and gets worse with rest; this is called the gelling phenomenon because it occurs when the synovial fluid becomes thickened, like a gel.
Other symptoms include joint instability, limited range of motion, and crepitus, which are crackling or popping sounds felt on joint palpation due to the bones rubbing against each other.
On examination, the osteophytes might be seen as single subcutaneous nodules over the affected joints. When seen in the distal interphalangeal joints, they are called Heberden nodes, and when they are seen in the proximal interphalangeal joints, they are called Bouchard nodes.
Osteoarthritis of the thumb is called rhizarthrosis. Now, because knee cartilage loss begins medially, individuals might have bowing of the affected knee.
Finally, unlike in rheumatoid arthritis, osteoarthritis doesn't cause systemic symptoms.For diagnosis, if osteoarthritis is suspected, plain x-rays of the most symptomatic joints should be taken.

Osteoarthritis Diagnosis29:45–30:55

X-rays generally reveal marginal osteophytes, narrowing of the joint space; increased density of the subchondral bone or osteosclerosis, which is seen as poorly defined areas within the bone that are whiter than the surrounding bone tissue; subchondral cysts, which are more common in osteoarthritis than rheumatoid arthritis; and joint effusions or increased amount of fluid within the synovial compartment.
Joint effusion of the knee is typically seen on a lateral radiograph as a well-defined rounded homogeneous soft tissue density within the suprapatellar recess.
Blood tests are normal in osteoarthritis, but are required to rule out rheumatoid arthritis or any underlying disorder causing secondary osteoarthritis.
If the individual presents with joint effusions, arthrocentesis and synovial fluid analysis can help differentiate it from other arthritides; in osteoarthritis, synovial fluid is usually clear, viscous, and has under 2000 white blood cells per microliter.Treatment of osteoarthritis can involve non-pharmacological approaches, like losing weight or moderate exercise, as well as physical therapy.

Osteoarthritis Treatment30:55–31:30

This can be especially important when large weight bearing joints like the hips and knees are affected. Pharmacological treatment focuses on reducing pain and inflammation, and it usually consists of acetaminophen and NSAIDs.
If neither of these are successful, some people might benefit from injections of hyaluronic acid or corticosteroids into the joint, or may need surgery to replace the affected joint.##SummaryAll right, as a quick recap… Rheumatoid arthritis is an inflammatory disease that causes progressive, symmetric destruction of at least three joints, especially the proximal interphalangeal joint, which leads to morning stiffness that lasts for more than an hour and improves with use.

Review31:30–33:28

Extra-articular symptoms include uveitis, pulmonary fibrosis, and rheumatoid nodules. Diagnosis is based on blood tests showing RF and anti-CCP, and on X-rays typical findings include juxta-articular osteopenia, soft tissue swelling, narrowing of the joint space, bone erosions, and subchondral cysts.
The long term treatment of rheumatoid arthritis is use of non-biological and biological DMARDs, while short term is with NSAIDs and glucocorticoids.
Juvenile idiopathic arthritis is an inflammatory disease that occurs in those under 16 years of age and there are three main types - oligoarticular arthritis, in which there are up to 4 joints affected; polyarticular arthritis, which affects 5 or more joints; and systemic juvenile idiopathic arthritis, which is also associated with systemic symptoms like fever, spiking rash, adenopathy, and splenomegaly.
Diagnosis is clinical, and treatment involves NSAIDs, intra-articular corticosteroids, and DMARDs. Osteoarthritis is caused by mechanical wear and tear, and it affects weight bearing joints.
It causes joint pain that worsens with activity and stiffening that lasts under 30 minutes and gets worse with rest. Diagnosis is based on X-rays, which reveal marginal osteophytes, narrowing of the joint space, subchondral bone osteosclerosis and cysts, and joint effusions.
Treatment consists of lifestyle changes and medication such as acetaminophen, NSAIDs, and injections of hyaluronic acid or corticosteroids.
Going back to our cases, Jody comes in with a 6 month history of bilateral hand and wrist stiffness that lasts for more than an hour a day but improves with use.

Summary33:28–34:36

Examination revealed swelling, limited range of movement, and rheumatoid nodules; and blood tests were positive for RF and anti-CCP.
Her symptoms, age, and the fact that she is seropositive for RF and anti-CCP is enough to make the diagnosis of rheumatoid arthritis.
Still, an X-ray scan of the affected joint might be needed to assess severity and disease progression. Kerry, on the other hand, is a 60 year old woman with a 1 year history of pain in the right knee that's worse with use and associated with stiffness, which typically occurs at rest and lasts for 15 minutes.
Examination revealed Kerry is obese, and his knee shows bowing and has a limited range of motion. Blood tests in Kerry's case were negative for both antibodies.
Now, given her age and the fact that she is obese, plus her symptoms and negative serology, we can easily diagnose Kerry with osteoarthritis.
An X-ray scan would be needed in her cases as
Rheumatoid arthritis and osteoarthritis: Video | Osmosis