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Arthritis Types

Contact Hours: 4

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Contact Hours: 4

This educational activity is credited for 4 contact hours at completion of the activity.

Course Purpose

The purpose of this course is to provide the healthcare professional with an overview of the types of arthritis, common symptoms, and management and treatment options.


Arthritis can severely impact an individual’s life and routine activities, and can also lead to inactivity-associated health conditions, such as obesity, cardiovascular disorders, and diabetes. This course will discuss the different types of arthritis, their treatments, and common management and treatment options.

Course Objectives

Upon completion of this course, the learner will be able to:

  • Describe the various types of arthritis
  • Describe common symptoms associated with the arthritis types
  • Identify modifiable factors to reduce the risk of arthritis
  • Review the available management and treatment options for arthritis
  • Review fibromyalgia, systemic lupus erythematosus and gout, and their preventative measures and treatment options

Policy Statement

This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.


Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.

Fast Facts: Arthritis Types

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Arthritis Types Pretest

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ArthritisThe swelling and tenderness of one or more joints.
Articular ChondrocytesA type of specialized connective tissue present in synovial joints.
FibromyalgiaA disorder that affects muscle and soft tissue characterized by chronic muscle pain, tenderness, fatigue and sleep disturbances.
GoutA common and complex form of arthritis that is characterized by sudden, severe attacks of pain, swelling, redness and tenderness in one or more joints, most often in the big toe.
HyperuricemiaElevated levels of uric acid, a waste product found in blood.
Juvenile Rheumatoid ArthritisAn inflammatory joint disease affecting children below 16 years that causes joint pain, swelling and stiffness.
Ligament TearAn injury caused by an extreme motion, like a forceful twisting of a joint. 
Monosodium Urate A salt of uric acid that precipitates out in cartilage as tophi in gout.
OsteoarthritisThe most common form of arthritis, also called degenerative joint disease or “wear and tear” arthritis.
Osteophyte(Bone spur) A tiny pointed outgrowth of bone, usually occurring at the joints where bones meet.
Pro-Inflammatory MarkersA marker of inflammation in the blood.
ProteasesAn enzyme which breaks down proteins and peptides.
PurinesA colorless crystalline compound with basic properties, forming uric acid on oxidation.
Rheumatoid ArthritisA chronic inflammatory disease that results in painful joints, swelling and stiffness in the joints.
Subchondral BoneA shock absorber in weight-bearing joints.
Synovium Inflammation(synovitis) When the synovium of a joint becomes inflamed. 
Systemic Lupus Erythematosus(SLE) An autoimmune disease, with systemic manifestations including skin rash, erosion of joints or even kidney failure.
Tophaceous DepositsA calcareous concretion formed in the soft tissue of a joint.
Uric AcidElevated levels of uric acid, a waste product found in blood.

Did you know that about 58.5 million people, around 1 in 4 adults in the United States, have doctor-diagnosed arthritis?1 Arthritis is defined as acute or chronic inflammation of the joints and encompasses various conditions that involve pain, limited movement, and swelling.2,3 Arthritis prevalence is also common in adults and individuals that are not physically active, around 23%, as compared to those that meet their physical activity recommendations; thus, it increases with age.1 It is also more common in women (23.5%) than men (18.1%)1.

Arthritis can severely impact an individual’s life and routine activities and can also lead to inactivity-associated health conditions, such as obesity, cardiovascular disorders, and diabetes.1 Despite the vast management and treatment options available; arthritis is a global health problem with serious consequences. For instance, it is projected that by 2040, around 78.4 million people will be diagnosed with arthritis.1 Moreover, the medical costs for arthritis treatment can add up to billions, especially in types that require replacement surgeries.4 Thus, the general public should be educated about the disorder and its preventive measures to help them lead an active lifestyle in the future. This course will discuss the different types of arthritis, their treatments, and common management and treatment options.

What is Arthritis?

Arthritis is a disease of the joints that affects individuals, especially adults.3 It includes multiple conditions that cause pain and inflammation of the joints, connective tissues, and tissues around the joints.5 Arthritis can be inflammatory or noninflammatory.3

There are multiple types of inflammatory arthritis, and they are caused by different factors, such as crystal deposition-induced inflammation, infections, or autoimmune disorders.3 On the other hand, inflammatory arthritis also comes with the burden of autoimmune connective tissue-associated diseases, such as celiac disease, scleroderma, systemic lupus erythematosus, myositis, and more.3

Arthritis can be acute or chronic, and treatment options are limited.2,3 More than 100 different types of arthritis have been identified, and the etiology, management, and treatment for each vary.2,5 The two most common types are osteoarthritis and degenerative arthritis.3

Types of Arthritis


Osteoarthritis (OA) is one of the most common forms of arthritis.6,7 It affects around 7% or 500+ million people worldwide, and was identified as the 15th highest cause of years lived with disabilities (YLDs) in 2019.7 Despite these concerning statistics, osteoarthritis prevalence is neglected, and its treatment has not made comparable progress with other non-communicable diseases.7 Osteoarthritis is a degenerative joint disorder and usually occurs in the knees, hands, and hips.9 It is associated with joint pain and loss of function and is further categorized into two types; primary and secondary osteoarthritis.6

Primary osteoarthritis is the most common subset of osteoarthritis and is diagnosed in the absence of a predisposing trauma or disease.6 In contrast, secondary osteoarthritis is diagnosed in individuals who have a preexisting joint abnormality.6 Predisposing trauma or conditions can include injury, metabolic disorders, congenital joint disorders, infectious arthritis, inflammatory arthritis, hemoglobinopathy, avascular necrosis, and more.6


Osteoarthritis is characterized by the following symptoms:3,6,8,9

  • Degeneration of ligaments and menisci of the knee
  • Hypertrophy of the joint capsule because of proteolytic enzymes
  • Inflammation and decreased range of motion
  • Osteophytes formation
  • Progressive articular cartilage loss and destruction
  • Subchondral bone thickening
  • Swelling and stiffness
  • Synovium inflammation in variable degrees

It is important to note that not all osteoarthritis patients may present with the above-listed symptoms. For instance, in the U.S., 80% of the population over 65 years old have radiographic evidence of osteoarthritis; however, only 60% of this subset exhibits symptoms.6 The reason is that radiographic osteoarthritis is two times as common as symptomatic osteoarthritis, and radiographic changes make it difficult to determine if the cause of joint pain is related to osteoarthritis.6


Osteoarthritis is a multi-factorial disease and is associated with gender, heredity, aging, joint injury, and obesity.3,6,7,8,9 Some genetic factors are also associated with osteoarthritis, such as mutations in genes encoding types II, IV, V, and VI collagens.3


  • Obesity has long been associated with osteoarthritis due to the increased body weight on load-bearing joints, such as the hips and knees.8,9 Obese patients diagnosed with OA have a higher risk of infection, more severe symptoms, and face technical difficulties in total joint replacement surgery.9
  • Obesity also causes metabolic changes that increase the risk of OA.9 For instance, the secretion of adipose tissue-derived cytokines, called adipokines, causes low-grade systemic inflammation.8 These inflammatory factors end up triggering the nuclear factor-κB (NF-κB) signaling pathway to stimulate an articular chondrocyte catabolic process and lead to extracellular matrix (ECM) degradation.8


  • As stated above, inflammation contributes to the progression and development of osteoarthritis and affects the cartilage, synovium, and subchondral bone.8 Inflammatory factors like IL-1β, TNF-α, and chemokines, are involved in this process.8


  • Aging is one of the most common factors associated with osteoarthritis.8,9 The risk of developing OA increases with age. Most often, adults over 65 years of age are diagnosed with OA or radiographic changes in their joints.8,9 Aging affects multiple joint tissues, such as cartilage, subchondral bone, and synovium.8 Studies focusing on articular chondrocytes conclude that aging cells present elevated oxidative stress that promotes cell senescence and alters mitochondrial function.8

Joint or Sports Injury

  • Any traumatic joint or sport-related injury can damage the cartilage, bone, or ligament and affect joint stabilization.8 Common injuries include ligament tear and strain, joint dislocation, and tissue tears.8 A study showed that 41%–51% of participants with previous knee injuries have radiographic signs of knee OA in later years.8


  • Individuals with a family history of OA are at a higher risk of developing osteoarthritis.8,9 Many studies have contributed to this statistic. For instance, genome-wide association screens (GWAS) have confirmed over 80 gene mutations or single-nucleotide polymorphisms (SNPs) involved in OA pathogenesis.8

All the causes mentioned above, along with mechanical stress, interplay and lead to pro-inflammatory markers and proteases that mediate joint destruction.6 However, the complete mechanism is complex and unknown.6

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that affects approximately 1% of people.3,10,11 In this disease, the body’s immune system attacks the healthy cells and causes inflammation in the affected areas.10 The disease initially affects smaller joints and then progresses to larger joints, and usually affects multiple joints at once, such as knees, wrists, and hands.10,11 In rheumatoid arthritis, the joints affected have an inflamed lining that causes damage to the joint tissue and can lead to deformity, chronic pain, ligament strains, weakened tendons and unsteadiness.10,11 Aside from joints, RA can also cause problems in other body parts, such as the eyes, heart, skin, kidneys, and lungs.10,11

Women are more likely to be diagnosed with rheumatoid arthritis in comparison to men and have a disease prevalence of 5% in those aged 65 and older.3 However, in rare circumstances, the disease may affect children as well. This condition is referred to as juvenile rheumatoid arthritis.11


Rheumatoid arthritis symptoms are more severe than osteoarthritis and are triggered by an autoimmune response to environmental factors.3 Rheumatoid arthritis symptoms also occur in flares when the symptoms worsen, and remission when symptoms resolve or become manageable.10 The following are the common symptoms associated with rheumatoid arthritis:3,10,11

  • Fatigue and tiredness
  • Fever and weakness
  • Morning stiffness in affected joints for more than 30 minutes
  • Pain in one or more joints
  • Same symptoms on both sides of the body, such as both knees and hands
  • Stiffness in one or more joints
  • Tender, swollen, or warm joints
  • Weight loss

If the symptoms last for 6 months or less, it is known as early RA. If the symptoms persist for more than 6 months, it is known as established RA.12 The disease can lead to increased mortality and morbidity if left untreated.12


Although the specific causes of rheumatoid arthritis are unknown, there are certain risk factors that increase risks of developing the disease.10 The following is a brief overview of potential causes.


  • Genetics plays a critical role in the development and progression of rheumatoid arthritis.10,11,12 Individuals with a family history of RA have a threefold to a ninefold chance of inheriting the disease.13 Moreover, several twin studies have revealed that genetic risk factors determine 50 to 60% of the risk of developing RA.13 In a nationwide study in the UK, of 91 monozygotic (MZ) and 112 dizygotic (DZ) twin pairs, the overall MZ concordance rate was 15%, and in dizygotic twins, 5%.12,13
    • The following are genes associated with increased risk of rheumatoid arthritis:12
      • CCR6 – C-C Motif Chemokine Receptor 6
      • CTLA4 – Cytotoxic T-Lymphocyte Associated Protein 4
      • HLA-DRB1 – HLA Class II BRB1 beta chain
      • IL2RA – Interleukin 2 Receptor Subunit Alpha
      • IRF5 – Interferon Regulatory Factor 5
      • PADI4 – Peptidyl Arginine Deiminase 4
      • PTPN22 – Protein Tyrosine Phosphatase Non-Receptor Type 22
      • STAT4 – Signal Transducer and Activator of Transcription 4
      • TRAF1 – TNF Receptor Associated Factor 1
    • Genetic polymorphism and epigenetics (heritable changes without altering the DNA sequence) are also associated with RA.12

Environmental Factors

  • Genetics is not the only risk factor associated with RA; several environmental, behavioral, and lifestyle behaviors also play a major role in RA development.13 Among them, smoking is the strongest and most consistent factor, with a clear dose-response associated with RA.12,13 It is believed that environmental factors interact with genetic factors in complex networks and facilitate RA’s development and progression.13 Several studies support this theory; for instance, a study has shown that there is an interaction between the shared epitope and smoking in anti-citrullinated protein antibody (anti-CCP) positive individuals.12
    • Other environmental factors include:12,13
      • Lower educational level (high risk)
      • High birth weight (high risk)
      • Obesity (high risk)
      • Moderate alcohol intake (low risk)
      • Breastfeeding (low risk)
  • Exposure to textile dust, silica, and asbestos also causes an autoimmune inflammatory response in the joints, which in turn affects the oropharynx, GI tract, and lungs.12,13 Any changes in the function or compositions of the intestinal microbiome are also associated with RA.12 The gut microbiome composition is altered in patients with rheumatoid arthritis (dysbiosis), where rheumatoid arthritis patients have decreased gut microbiome diversity compared with healthy individuals.12

Once called the king of diseases and disease of kings, gout is the most common inflammatory arthritis in adults in the U.S., even more so than rheumatoid arthritis.14,15 It causes swelling of the joints and is extremely painful.16 Initially, it affects the bigger joints, such as the big toe or lower limb.16 Gout symptoms occur in flares where the symptoms worsen, followed by a period of remission when the symptoms resolve or lessen.16,17

Gout prevalence is higher in ethnic and racial minorities; for instance, the Johns Hopkins Precursors study and the Meharry cohort study concluded that the incidence of gout was 3.11 in African American men versus 1.82 per 1000 person-years in White men (P < 0.05); respectively, the cumulative incidence was 10.9% and 5.8% (P = 0.04).14

Gout occurs from the concentration of the end product of human purine metabolism, the monsodium urate (MSU) crystals in bones, joints, and soft tissues.15 When the serum urate level builds up in the body, it forms MSU crystals around the joints, causing inflammation and arthritis.16 This can happen if the body is inefficient in removing urate or produces an excess amount; however, not all individuals with high urate serum levels develop gout.16

The disease progresses through a series of stages:15,16

  • Acute gout flare (recurrent flares of inflammatory arthritis)
  • Chronic gouty arthropathy
  • Accumulation of urate crystals in the form of tophaceous deposits
  • Uric acid nephrolithiasis
  • Chronic nephropathy

Currently, there is no cure for gout, but symptoms can be managed through medication and self-management strategies.17 Despite being the most common, it is the most controllable form of arthritis and can be effectively managed through early diagnosis and lifestyle changes.16


As stated above, there are times when the symptoms are severe, called flares, that can last for days or weeks followed by a period of remission, when the symptoms resolve for months or years.17 Gout usually affects one joint at a time, aside from the big toe or lower limb; other body parts affected by gout include tendon sheaths, bursae, and kidneys.16,17

The following are some of the common symptoms of gout:16,17

  • Pain in the affected joints.
  • Swollen, warm, and stiff joints (flares usually occur at night).
  • Gout can develop as a secondary condition from other health conditions in patients, such as obesity, diabetes, hypertension, chronic kidney disease, myocardial infarction, and congestive heart failure.


Gout is caused by a condition known as hyperuricemia.15,16,17 It is the leading cause of gout and occurs when there is excess uric acid levels in the body.15,16,17 Purines are compounds that are naturally found in the body and the food that is consumed. When the body breaks down purines, it produces uric acid. When uric acid builds up in the body, it forms urate crystals, also known as monosodium urate, around the joints, fluids, and tissues in the body and causes inflammation.16,17

Individuals with hyperuricemia are at a higher risk of gout flare-ups.15 For instance, in a study involving 2000 older adults with gout, participants with 9 mg/dl or more urate levels were three times more likely to have a flare over the next 12 months than those with levels less than 6 mg/dl.15

The following are some of the causes of hyperuricemia or urate overproduction in the body:15

  • Clinical disorders
    • Down syndrome
    • Hemolytic disorders
    • Insulin-resistance syndrome
    • Malignancies
    • Obesity
    • Tissue hypoxia
  • Drug, diet, or toxin-induced
    • 4-amino-5-imidazole carboxamide riboside
    • Cytotoxic drugs
    • Ethanol
    • Fructose
    • Pancreatic extract
    • Vitamin B12 deficiency
  • Inherited enzyme defects
    • Glucose-6-phosphatase deficiency (glycogen storage disease, type I)
    • Hypoxanthine-guanine phosphoribosyltransferase deficiency
    • Phosphoribosylpyrophosphate synthetase overactivity

Aside from hyperuricemia, there are multiple dietary, environmental, and genetic risk factors that can increase one’s chances of developing gout, such as15,16,17

  • Age, gender, ethnicity, and genetic variants
  • Alcohol
  • Chronic kidney disease
  • Diabetes mellitus
  • Family history of gout
  • Having a high-purine diet
  • High blood pressure
  • Hyperlipidemia
  • Medications altering urate balance

Fibromyalgia is a pain regulation disorder that is characterized by chronic and widespread musculoskeletal pain.18,19 It has a high prevalence rate in the United States, around 6.4%, and is more common among women (7.7% in women and 4.9% in men).18,20 The reason why this disease is more common in women than men is the higher level of depression and anxiety, hormonal changes due to the menstrual cycle, and the use of maladaptive methods to cope with pain.18

It is associated with pain and tenderness throughout the body and also results in difficulty sleeping and fatigue.21 The exact cause and pathophysiology of the disease are unknown, but researchers believe it is related to a pain-processing problem in the brain, which leads to heightened sensitivity to pain.19,21 The constant burden of pain is also associated with certain neurological and psychiatric conditions.18,19

Following are the alterations commonly observed in patients with fibromyalgia:18,19

  • Dysfunction in the mono-aminergic neurotransmission, resulting in elevated levels of the excitatory neurotransmitters like glutamate and substance P
  • Decreased levels of serotonin and norepinephrine in the descending antinociceptive pathways in the spinal cord
  • Prolonged enhancement of pain sensations
  • Dopamine dysregulation
  • Alteration in the activity of endogenous brain opioids.

The pain sensitivity observed in fibromyalgia can be linked to the central nervous system and peripheral pain generators.19 Moreover, according to research, fibromyalgia patients undergo a principle called “cognitive-emotional sensitization,” which shows how selective attention to specific body parts can increase that pain perception.19


The following are some of the common symptoms associated with fibromyalgia18,19,21

  • Aching, throbbing, or burning pain sensation
  • Bloating and constipation
  • Cognitive disturbances, including rapidly changing thoughts and difficulty focusing
  • Depression and anxiety
  • Fatigue (when waking up or during mid-afternoon)
  • Headaches; migraines and tension-type
  • Heightened sensitivity to temperature, light, noise, and odor
  • Intestinal irritability
  • Joint stiffness
  • Mood disorders
  • Trouble sleeping
  • Widespread musculoskeletal pain (bilateral pain in both upper and lower body parts. The pain may initially be localized in the shoulders and neck)


As stated above, the exact cause of fibromyalgia is unknown and complex; however, it is thought to be a central and peripheral nerve disorder.19 Aside from these, the following factors are also considered plausible causes.


  • Many studies have shown a correlation between genes and fibromyalgia.19 For instance, a genome-wide linkage scan study concluded that first-degree relatives had an increased risk of developing the disease.19 Moreover, there is a 50% correlation rate between chronic pain and genetic variants. The two major genes responsible for pain sensitivity and susceptibility in fibromyalgia are the serotonin transporter gene (SLC64A4) and the transient receptor 2 potential vanillic channel gene (TRPV2). SLC64A4 is characterized by a single nucleotide polymorphism and is associated with chronic pain conditions and increased levels of depression and psychological disorders related to an alteration in serotonin reuptake.19

Inflammation and Immune System

  • Several studies also support the theory that inflammatory processes in the peripheral tissues, brain, and spinal cord cause fibromyalgia.19 Patients with fibromyalgia experience symptoms like dysesthesia, swelling, fatigue, and cognitive disturbances, which are the result of the release of chemokines and cytokines that cause innate and adaptive immune system activation.19 Moreover, neurogenic inflammation in fibromyalgia is also increased by stress, emotions, and other psychological mechanisms.19

Endocrine Factors

  • Several endocrine factors were also studied throughout the years; for instance, individuals with fibromyalgia were analyzed based on the levels of corticotropin-releasing factor (CRF) in cerebrospinal fluid (CSF), heart rate variability (HRV), and pain symptoms. The results concluded that sensory and affective pain symptoms were associated with CRF levels but not fatigue.19
Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is the most common form of lupus and is an autoimmune disease involving multiple systems.22,23 In SLE, the immune system attacks healthy cells and causes inflammation and pain in the affected body parts.23 It has multiple phenotypes and can progress from mild to multiorgan and central nervous system involvement.22

The disease is more common among African Americans, and the onset usually occurs at an early age.22 It is also more common among females than males, with a ratio of 9:1.22 However, the risk of developing SLE reduces in women after menopause.22 Systemic lupus erythematosus is also prevalent in children and is found to be more severe in children.22

The exact cause of SLE is unknown, and the pathophysiology is constantly evolving.22,23 It is known to affect the joints, lungs, kidneys, blood vessels, brain, and skin.23


Lupus can affect any body organ, and symptoms may vary from person to person.23 The following are common symptoms associated with SLE:23

  • Anemia
  • Chest pain
  • Eye diseases
  • Fever
  • Forgetfulness and confusion
  • Hair loss
  • Heightened sensitivity to light
  • Mouth ulcers
  • Pain and swelling in the joints
  • Skin rashes

These symptoms can affect an individual’s mental, physical, and social functioning, and affect their quality of life.23 Adults with lupus have periods of severe symptoms called flares and remission periods when the symptoms resolve for months or years.23


The exact cause of SLE is unknown, but several environmental, genetic, endocrine, and immunological factors play a significant role in its development.22

Several genes have been identified that are associated with SLE; for instance, over 100 gene loci with polymorphisms are associated with polygenic SLE, and more than 30 genes causing monogenic forms of SLE or SLE-like.22

Moreover, female sex and hormonal changes are also risk factors.22 Estrogen hormone causes the release of specific cytokines, T and B cells, thymocytes, and macrophages, and regulates the expression of HLA; all of which promote autoimmunity.22 Moreover, utilization of postmenopausal hormone replacement therapy or contraceptives can cause flares in SLE patients and increase the risk of SLE.22

Aside from this, drugs like procainamide and hydralazine are causing lupus-like phenomena by causing the demethylation of DNA and alteration of self-antigens.22

Treatment Options


Currently, there is no cure for osteoarthritis (OA), and treatment goals involve limiting pain and improving functional loss.3,6,9 Healthcare professionals recommend using a combination of pharmacological and non-pharmacological therapies for optimal care based on the disease’s progression.3,6,9

Non-Pharmacological Options

Non-pharmacological therapies are suited for individuals with mild symptoms and include the following:3,6

  • Avoid activities or lifting weights that cause extreme pain or overload the joints
  • Perform specific exercises to improve strength
  • Utilize occupational therapy to unload joints via cane, brace, crutch, or splint.
  • Weight loss treatments

Physical therapy is useful for OA patients as it helps them get used to supportive devices, such as canes or crutches, and also educates them on the right type of exercises based on their limited abilities.6 Many healthcare professionals recommend exercise programs that include both aerobic and resistance training as it has been shown to improve physical function and limit pain.6 Moreover, misaligned joints should be corrected by braces or orthotics or other mechanical means.6 However, for OA individuals who are overweight or obese, weight loss is the best treatment option; it helps unload the joints and knees by 3 to 6-fold.6,9

Pharmacological Options

Pharmacological treatment options for OA involve oral and topical drugs and injections.3,6 Remember that OA is associated with the degradation of articular cartilage and bone matrix components.24 Thus, the cartilage matrix degenerations products are highly researched for target drugs.24 This is because multiple anabolic and catabolic pathway enzymes are abnormally regulated in osteoarthritis cartilage, offering researchers the option to identify and validate new drugs.24

Usually, the common drugs recommended for OA include non-steroidal anti-inflammatory drugs (NSAIDs), both oral and topical, duloxetine, and topical capsaicin.3,6 NSAIDs are an affordable and popular option that is prescribed orally and topically and taken when needed rather than on a schedule.3,6 Oral NSAIDs have significant cardiovascular, renal, and gastrointestinal side effects that require constant monitoring.6 Topical NSAIDs have fewer side effects but are less effective and can cause skin irritation.6

Each person reacts differently to treatment regimens.6 If OA patients are unresponsive to pharmacological and non-pharmacological options, replacement surgery is considered.3,6 Knee and hip replacement surgery has low failure rates and can provide instant relief and improved functionality; however, patients may experience post-surgical complications and limited movement post-surgery for a period of time.3,6 Physical therapy is also required post-surgery.3

Rheumatoid Arthritis

Rheumatoid arthritis can be effectively managed and treated with the help of medication and other self-management therapies, with surgery being the last option.10,11 The aim of RA treatment is to reduce joint deformity, reduce joint pain and inflammation, and improve functionality.11 Treatment plans are designed based on a patient’s overall health and disease progression.11 Following are the treatment options available for RA:

NSAIDs and Corticosteroids

  • First-line treatment for RA involves NSAIDs that are targeted toward reducing joint pain and inflammation.11,12 There are more than 20 NSAIDs available on the market for joint treatment, among which aspirin is the oldest, although certain side effects, such as gastric intolerance, tinnitus, and hearing loss, are associated with high doses of aspirin.11 NSAIDs can also cause gastrointestinal, renal, and hematologic toxicity; thus, the choice of the drugs depends on the patient’s comorbidities.12
    • Common NSAIDs for RA include:11
      • Acetylsalicylate (Aspirin)
      • Etodolac (Lodine)
      • Ibuprofen (Advil and Motrin)
      • Naproxen (Naprosyn)
  • Corticosteroids
    • Corticosteroids are another class of anti-inflammatory drugs that are used in RA patients during flares or active RA.11,12 They are also used as bridge therapy when disease-modifying antirheumatic drugs (DMARD)  therapy is being instituted.12 However, corticosteroids have more side effects and are thus only administered in small doses for a short period.11 Long-term side effects of corticosteroids are11,12
  • Bone-thinning or osteoporosis
  • Diabetes
    • Immunosuppression
    • Weight gain
  • Disease-Modifying Antirheumatic Drugs (DMARDs)
    • Disease-modifying antirheumatic drugs (DMARDs) are the second-line treatment for RA patients.10,11 These drugs help promote remission by slowing down the progression of joint deformity.11 Although, these drugs help promote RA remission, they are slow-acting and can take weeks or months to show effective results.11 One of the initial drugs recommended from this class is methotrexate.11,12 Usually, the treatment plan involves an initial dose of 10-15 mg/week of methotrexate with an escalation of 5 mg/month and a target dose of 20-25 mg/week.12 Subcutaneous administration is recommended for patients who are intolerant to oral administration.12 Other drugs included in this category are hydroxychloroquine (HCQ), leflunomide, azathioprine (AZA), sulfasalazine, and cyclosporine.12
  • Surgery 
  • Surgery is considered a last resort for RA patients when no other treatment bears fruitful results.11 Surgery options include:11
    • Arthroscopy – Repair of ruptured tendons.
    • Joint Fusion – Performed to stabilize joints that are not easily replaceable, such as the ankle, thumb, wrist, and cervical spine.
    • Osteotomy – Weight-bearing bones are realigned to correct valgus or varus deformities, most commonly in the knee.
    • Radiosynovectomy – An alternative to surgical synovectomy and is more cost-effective than other surgical options. It involves an intra-articular injection of small radioactive particles and is used to treat multiple joints simultaneously.
    • Tenosynovectomy – Involves the excision of inflamed tendon sheaths or repairing a recent tendon rupture, most commonly in hand.


Treatment plan for gout depends on the causes of gout and the patient’s overall health and symptoms.16 However, the goal of every treatment is the same, such as reducing symptoms and inflammation and preventing future flares.15,16

Treatment for acute gout flare involves pharmacological and non-pharmacological therapies.15 Healthcare professionals start treatment within 48 hours of the first signs of symptoms to reduce severity and pain.15

Non-pharmacological therapy involves applying ice packs in combination with medication to reduce inflammation.15 Moreover, there are several drugs used as a first-line treatment.15 These treatments span 7 to 10 days to eliminate flare-ups.15

Table 2: Pharmacological options for acute gout flare15,16

NSAIDsCelecoxib (200 mg twice daily). Diclofenac (50 mg two to three times daily ibuprofen (800 mg three times daily) Indomethacin (50 mg three times daily) Meloxicam (15 mg daily) Naproxen (500 mg twice daily)Treatment lasts 5 to 7 days Side effects include cardiovascular, renal, and gastrointestinal toxicity.
Oral GlucocorticoidsPrednisolone or prednisone (30 to 40 mg once daily or given in a divided twice-daily dose until flare resolution begins) Triamcinolone (60mg once) or methylprednisoloneFor patients with contraindications to NSAIDs and/or colchicine Highly recommended for patients with renal insufficiency Side effects include mood changes, increased fluid retention, high blood pressure, and hyperglycemia.
Parenteral GlucocorticoidsMethylprednisolone ( 20 mg intravenously twice daily, with stepwise reduction and rapid transition to oral prednisone when improvement begins.) Adrenocorticotropic hormone (ACTH)Suggested for patients who cannot take oral medications or are not candidates for intra articular glucocorticoid injection.
ColchicineNo more than 0.3 mg dose is administered on the day of a gout flare, and the dose is not repeated for at least three to seven days or more in high-risk patientsShown to reduce pain by 50% in an RCT.


There is no definite cure for fibromyalgia, but different non-pharmacological, pharmacological, and self-management therapies are available for management.18,21


Cardiovascular fitness training is recommended for FM patients for pain management and improving sleep.18 This includes 30 minutes of aerobic exercise, 3 times a week, with a set heart rate target range.18 For patients who cannot perform low-impact aerobic exercises, healthcare professionals recommend enrolling in a supervised exercise program.18 In some studies, yoga and water-based exercise are also helpful.18


Medications for FM involve anti-seizure medicines, antidepressants, and pain-relieving drugs.21 Therapy is initiated using antidepressants, which include tricyclic medications like amitriptyline, selective serotonin reuptake inhibitors (SSRIs), and norepinephrine reuptake inhibitors (SNRIs), including duloxetine and milnacipran.18 These drugs are used in combination with non-pharmacological treatment options to ensure optimal care and management.18 The FDA has also approved three drugs for FM management; pregabalin, duloxetine, and milnacipran.18


Antioxidants and vitamins are also used for the treatment of FM because of the higher number of harmful free radicals produced in FM.19

Table 3: Compounds with antioxidant and analgesic properties for FM management19

MelatoninIn an animal study, melatonin improved behavioral defects, oxidative and nitrosative stress, mast cell infiltration and activation of microglia in a reserpine-induced FM model.
Coenzyme Q10CoQ10 supplementation provided benefits like relieving pain sensation in FM patients treated with pregabalin (by improving mitochondrial function, reducing inflammation, and decreasing brain activity)
Vitamins D and EA clinical study found that women with FM had a lower qualitative and quantitative intake than control subjects. An association has been found between vitamin D deficiency and FM. However, its role in FM pathophysiology and clinical relevance requires further studies. Only vitamin E appears to be related to the quality of life and pain sensation.

Systemic Lupus Erythematosus (SLE)

Treatment and management of SLE depend upon the number of organs involved and the progression of the disease.22,23 Treatment can range from NSAIDs, antimalarial drugs, and immunosuppressives to corticosteroids and cytotoxic drugs.22,23

The following are the drugs recommended based on different manifestations:22

Table 4: SLE management drugs for different manifestations22

Hematological manifestationsAzathioprine or cyclosporine-A can be used as a steroid-sparing agent. Corticosteroids are the primary treatment option.
Musculoskeletal manifestationsHydroxychloroquine (initial drug choice). If no response, methotrexate or leflunomide can be considered. In refractory cases, belimumab and rituximab are considered.
CNS manifestationsHigh-dose corticosteroids are used with immunosuppressive agents such as cyclophosphamide, azathioprine, or rituximab.
Renal manifestationsRenin-angiotensin-aldosterone system blockade is used for treating Class I and II LN Immunosuppression with high-dose corticosteroids followed by azathioprine is indicated only if proteinuria is more than 1 gram/day. Membranous LN (class V) shall also be treated with the Renin-angiotensin-aldosterone system blockade
Pregnancy manifestationsHydroxychloroquine is considered safe in pregnancy and has shown positive results in reducing flares and disease activity and can be continued through pregnancy. Azathioprine and low-dose corticosteroids are also used for mild manifestations.
Preventive Measures

Unfortunately, there is no way to prevent arthritis. However, there are certain measures that can be taken to control its symptoms or delay its onset.25,26 Every arthritis type has different modifiable risk factors. For instance, by maintaining a healthy weight and diet, the risks of osteoarthritis and gout may be reduced, and avoiding smoking can reduce the risk of rheumatoid arthritis.26 For individuals with genetic predisposition, the discovery and awareness of certain environmental triggers and toxins can also delay its onset.26

The center for disease control recognizes five self-management strategies to prevent arthritis and its symptoms:25

  • Learn new self-management skills by joining an education workshop
  • Be active to maintain a drug-free life
  • Consult a doctor and getting an early diagnosis
  • Manage weight to reduce stress on joints
  • Protect joints by choosing activities that do not put an extreme load on them, such as swimming, cycling, walking, etc. 

Arthritis is a health problem that can have severe systemic repercussions.3 As stated above, there is no cure for arthritis, and only self-management techniques, medications, and exercises are employed to help reduce pain and inflammation.3 The American College of Rheumatology recommends an interprofessional approach to arthritis treatment and management to improve overall health related to the diagnosis.3

Patients should also be educated on the etiology and pathophysiology of their specific arthritis type, along with the lifestyle modifications they should make to manage the symptoms.6 Almost all people with arthritis benefit from physical interventions and exercise programs, among which water-based activities and yoga can help reduce joint pain and inflammation.3 Patients should also be advised to maintain a healthy weight by choosing a diet that is low in sugar, alcohol, and purines.3,26 Arthritis is manageable and patients should be educated about the preventive measures and symptoms for early diagnosis and symptom management.3

  1. Centers for Disease Control and Prevention. National Statistics. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/arthritis/data_statistics/national-statistics.html
  2. Arthritis. www.hopkinsmedicine.org. https://www.hopkinsmedicine.org/health/conditions-and-diseases/arthritis
  3. ‌Shayan Senthelal, Thomas MA. Arthritis. Nih.gov. Published November 14, 2018. https://www.ncbi.nlm.nih.gov/books/NBK518992/
  4. ‌Arthritis Cost Statistics. Published 2019. https://www.cdc.gov/arthritis/data_statistics/cost.htm
  5. ‌CDC. Arthritis Types. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/arthritis/basics/types.html
  6. ‌Sen R, Hurley JA. Osteoarthritis. PubMed. Published 2022. https://www.ncbi.nlm.nih.gov/books/NBK482326/#article-26373.s2
  7. ‌Hunter DJ, March L, Chew M. Osteoarthritis in 2020 and beyond: a Lancet Commission. The Lancet. 2020;0(0). doi:10.1016/S0140-6736(20)32230-3
  8. ‌Chen D, Shen J, Zhao W, et al. Osteoarthritis: toward a comprehensive understanding of pathological mechanisms. Bone Research. 2017;5(1):1-13. doi:10.1038/boneres.2016.44
  9. ‌Centers for Disease Control and Prevention. Osteoarthritis (OA). Centers for Disease Control and Prevention. Published July 27, 2020. https://www.cdc.gov/arthritis/basics/osteoarthritis.htm
  10. ‌Centers for Disease Control and Prevention. Rheumatoid arthritis (RA). centers for disease control and prevention. Published July 27, 2020. https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html
  11. ‌Karger.com. Published 2020. https://www.karger.com/Article/FullText/493390
  12. ‌Chauhan K, Jandu JS, Al-Dhahir MA. Rheumatoid Arthritis. PubMed. Published 2022. https://www.ncbi.nlm.nih.gov/books/NBK441999/
  13. ‌van der Woude D, van der Helm-van Mil AHM. Update on the epidemiology, risk factors, and disease outcomes of rheumatoid arthritis. Best Practice & Research Clinical Rheumatology. 2018;32(2):174-187. doi:10.1016/j.berh.2018.10.005
  14. ‌Singh JA, Gaffo A. Gout epidemiology and comorbidities. Seminars in Arthritis and Rheumatism. 2020;50(3):S11-S16. doi:10.1016/j.semarthrit.2020.04.008
  15. ‌Fenando A, Widrich J. Gout. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK546606/
  16. ‌NIAMS. Gout. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Published April 12, 2017. https://www.niams.nih.gov/health-topics/gout
  17. ‌CDC. Gout | Arthritis | CDC. www.cdc.gov. Published July 27, 2020. https://www.cdc.gov/arthritis/basics/gout.html#:~:text=quality%20of%20life%3F-
  18. ‌PMC E. Europe PMC. europepmc.org. Accessed January 27, 2023. https://europepmc.org/article/NBK/nbk540974#_article-65391_s3_
  19. ‌Siracusa R, Paola RD, Cuzzocrea S, Impellizzeri D. Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update. International Journal of Molecular Sciences. 2021;22(8):3891. doi:10.3390/ijms22083891
  20. ‌Marques AP, Santo A de S do E, Berssaneti AA, Matsutani LA, Yuan SLK. Prevalence of fibromyalgia: literature review update. Revista Brasileira de Reumatologia (English Edition). 2017;57(4):356-363. doi:10.1016/j.rbre.2017.01.005
  21. ‌Nancy Garrick DD. Fibromyalgia. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Published April 5, 2017. https://www.niams.nih.gov/health-topics/fibromyalgia#:~:text=Fibromyalgia%20is%20a%20chronic%20(long
  22. ‌Justiz Vaillant AA, Goyal A, Bansal P, Varacallo M. Lupus Erythematosus. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK535405/
  23. ‌CDC. Systemic Lupus Erythematosus (SLE). Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/lupus/facts/detailed.html
  24. Grässel S, Muschter D. Recent advances in the treatment of osteoarthritis. F1000Research. 2020;9(1). doi:10.12688/f1000research.22115.1
  25. 5 Proven Ways to Manage Arthritis. centers for disease control and prevention. Published 2019. https://www.cdc.gov/arthritis/basics/management.htm
  26. ‌How to Reduce Your Risk of Arthritis | Arthritis Foundation. www.arthritis.org. https://www.arthritis.org/health-wellness/about-arthritis/understanding-arthritis/reduce-your-risk
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