Causes of Rheumatoid Arthritis

If you’ve ever walked out of a doctor’s office thinking, “Okay, but why did I get rheumatoid arthritis in the first place?”you’re not alone. RA is a common autoimmune disease, yet even in 2025 there isn’t a single neat answer like “it’s this one virus” or “it’s because you ate that one cheeseburger.” Instead, the causes of rheumatoid arthritis look more like a puzzle: genetics, immune system glitches, hormones, lifestyle, and environmental exposures all snapping together in slightly different ways for each person.

In this guide, we’ll break down what scientists know (and don’t know) about the causes of rheumatoid arthritis, what actually counts as a risk factor, and what you can do to stack the odds a little more in your favorwithout needing a PhD in immunology.

Quick reminder: This article is for general information only and doesn’t replace medical advice. If you’re worried about your joints, symptoms, or risk, talk with a rheumatologist or another qualified health professional.

What Is Rheumatoid Arthritis, Really?

Rheumatoid arthritis (RA) is a chronic autoimmune disease. Instead of just defending you against germs, your immune system starts attacking the lining of your joints (the synovium). That attack leads to inflammation, pain, swelling, andover timedamage to cartilage and bone. RA often affects the small joints in your hands and feet first and tends to show up symmetrically (both wrists, both knees, etc.). It can also affect organs like the lungs, heart, eyes, and blood vessels.

The key word here is autoimmune: your immune system is misreading your own tissues as “the enemy.” Understanding why that misread happens is where the “causes of rheumatoid arthritis” story gets interesting.

Why Doctors Say “We Don’t Know the Exact Cause”

If you ask a rheumatologist what causes RA, they’ll usually say something like, “We don’t know the exact cause, but we know it’s a combination of factors.” That’s not a cop-out; it’s the honest state of the science.

Researchers are pretty confident about three big ideas:

• Genes matter. Certain genetic patterns, especially in immune-related genes, raise your risk.
• The environment matters. Smoking, air pollution, some infections, and possibly gum disease can act as triggers in people who are genetically susceptible.
• Hormones and life events matter. RA is more common in women, and pregnancy, childbirth, and menopause all seem to influence risk.

In other words, most people don’t get RA from a single cause. Instead, your genes load the gun, your environment cocks it, and some life eventlike an infection or stresspulls the trigger.

How the Immune System Goes Off Track

Autoimmune misfire 101

Under normal circumstances, your immune system is good at telling “you” from “not you.” With RA, that system gets confused. Your body starts producing autoantibodies like rheumatoid factor (RF) and anti–cyclic citrullinated peptide (anti-CCP or ACPA). These antibodies target your own tissues, especially in the joints, where they fuel inflammation.

Scientists think this misfire starts years before RA symptoms show up. Some people test positive for these antibodies long before they ever feel joint pain. During this “pre-RA” phase, something in the lungs, gums, or gut may be quietly stirring up the immune system.

Inflammation that refuses to shut off

Once the autoimmune process is underway, immune cells flood the joint lining and spit out inflammatory chemicals called cytokines (think TNF, IL-6, and friends). These cytokines tell more immune cells to pile in, and the joint becomes a crowded, angry place. Over time, this chronic inflammation erodes cartilage and bone and can even spread beyond the joints.

This runaway inflammation isn’t the “cause” in the sense of a starting point, but it’s the main reason RA can be so destructive if it isn’t treated early and aggressively.

Genetic Causes: The Loaded Dice You Inherited

RA is not purely genetic, but genetics play a major role. Having a close family member with rheumatoid arthritis increases your risk, and large studies suggest that roughly half of RA risk may be related to inherited factors.

The HLA “shared epitope” story

One of the strongest genetic risk factors involves immune-system genes known as HLA-DRB1. Certain versions of these genes share a small sequence of amino acids called the “shared epitope.” People who carry these versions are more likely to develop RA, especially the type that’s positive for anti-CCP antibodies.

Why does that matter? These HLA molecules help present pieces of proteins to immune cells. The “shared epitope” seems particularly good at presenting citrullinated proteinsproteins that have been chemically modified in a way that appears to trigger RA in vulnerable people.

Other genes that nudge your risk

HLA genes are just the headline. Dozens of other genes are involved, many of them controlling how inflammation is turned on and off. These genes might affect:

• How strongly your immune system responds to infection
• How easily your tissues become inflamed
• How your body clears damaged cells and proteins

The important takeaway: genetics can raise your odds of getting rheumatoid arthritis, but they don’t guarantee it. Plenty of people with “high-risk” genes never develop RA, and many people with RA don’t have a strong family history.

Environmental Triggers: When the Outside World Piles On

Genes set the stage, but environmental factors often decide if and when RA shows up. Several triggers and exposures have been linked to higher RA risk, especially in people who already have genetic susceptibility.

1. Smoking: The biggest preventable risk factor

If rheumatoid arthritis had a “most wanted” poster, cigarette smoking would be front and center. Smoking doesn’t just irritate your lungs; it also seems to promote citrullination and other chemical changes in proteins, especially in lung tissue. For people with certain HLA-DRB1 genes, this combination can dramatically increase RA risk.

Studies show that:

• Long-term smokers have a significantly higher risk of developing RA, particularly the anti-CCP positive type.
• Heavy smoking may raise RA risk several-fold compared with non-smokers.
• Quitting smoking gradually reduces risk, although it can remain somewhat higher than in people who never smoked.

What about vaping? Research is still evolving, but anything that chronically inflames the lungs is unlikely to be your joints’ best friend.

2. Air pollution and occupational exposures

It’s not just cigarettes. Long-term exposure to air pollution and certain dusts appears to increase RA risk as well. Tiny particles and chemicals inhaled into the lungs may trigger local inflammation and immune changes similar to those seen with smoking.

Higher risk has been linked to:

• Urban air pollution and fine particulate matter
• Occupational exposure to silica dust (for example, in mining, sandblasting, or some construction jobs)
• Other industrial dusts and fumes in certain workplaces

Again, this doesn’t mean everyone exposed will get RA, but it’s another piece of the gene–environment puzzle.

3. Infections and the microbiome

Scientists have long suspected that infections might trigger autoimmune diseases in people with the right genetic background. For RA, the evidence is less about one specific germ and more about how your microbiomethe bacteria in your mouth and gutinteracts with your immune system.

Two areas get a lot of attention:

• Gum disease (periodontitis). People with rheumatoid arthritis are more likely to have serious gum disease, and certain bacteria like Porphyromonas gingivalis may promote citrullination and autoantibody formation.
• Gut bacteria. Some studies suggest that shifts in gut microbes happen before RA develops, potentially nudging the immune system toward autoimmunity.

Does this mean flossing will “cure” RA? No. But good oral hygiene and regular dental care are increasingly seen as part of a smart prevention and management strategy, especially if you’re already at higher risk.

4. Hormones, pregnancy, and reproductive history

RA is about two to three times more common in women than men, and symptoms often first appear between ages 30 and 60. That pattern has turned a lot of scientific attention toward sex hormones, especially estrogen and progesterone.

Researchers have noticed that:

• Some women notice RA symptoms improve during pregnancy and flare after delivery.
• Never having given birth may be associated with higher RA risk in some studies.
• Menopause and changing hormone levels may influence when RA appears.

The exact hormonal “recipe” behind these patterns isn’t fully understood. But it’s clear that reproductive history and hormone shifts are part of the RA risk picture, especially for women.

5. Weight, diet, and overall lifestyle

Obesity doesn’t cause RA by itself, but carrying extra weight can increase inflammatory markers and may raise the risk of developing rheumatoid arthritis. Adipose tissue (body fat) is biologically activeit releases hormones and cytokines that can keep the body in a low-grade inflammatory state.

Diet and physical activity also play supporting roles. Diets high in ultra-processed foods and low in fruits, vegetables, and healthy fats may contribute to systemic inflammation, while regular movement and a nutrient-dense eating pattern support overall immune health. None of these lifestyle factors are magic shields, but they do influence how “inflammatory” your internal environment is.

Other Risk Factors You Can’t Control

Some risk factors for rheumatoid arthritis are completely out of your handsbut they still help explain who tends to get RA and when it tends to appear.

• Age: RA can start at any age, but it’s most common in adults in midlife and beyond.
• Sex: Women are significantly more likely to develop RA than men.
• Family history: Having a parent, sibling, or other close relative with RA raises your risk.
• Ethnicity: Some populations (such as certain Native American groups) have higher RA prevalence, likely due to differences in genetic risk.
• Early life exposures: Growing up in a smoking household or in lower-income environments has been linked to higher RA risk later in life.

You can’t go back and pick different parents, but knowing these risk factors can help you and your doctor decide how closely to monitor new joint symptoms or autoantibody test results.

What Does Not Cause Rheumatoid Arthritis?

Let’s clear up a few myths while we’re here. These things may affect symptoms, but they don’t actually cause rheumatoid arthritis:

• Cracking your knuckles. Annoying to others? Possibly. Cause of RA? No.
• Cold weather. Cold may make joints feel stiffer, but it doesn’t create RA from scratch.
• Minor injuries. A sprained ankle or jammed finger might reveal an already-inflamed joint, but it’s not considered a root cause.
• Stress alone. Life stress can make pain and fatigue worse and might act as a trigger in some people, but it’s not viewed as a stand-alone cause.

Also worth noting: rheumatoid arthritis is very different from osteoarthritis (the “wear-and-tear” type of arthritis). Overusing your joints might contribute to osteoarthritis over time, but RA is driven by the immune system, not by simple mechanical wear.

Can You Prevent Rheumatoid Arthritis?

There’s currently no guaranteed way to prevent RA, especially if you have strong genetic risk. But you can lower your overall risk or potentially delay onset by focusing on modifiable factors:

• Don’t smokeand quit if you do. This is the single biggest step you can take for RA risk, not to mention heart and lung health.
• Limit lung irritants. If you work around dusts, fumes, or chemicals, use protective gear and follow safety guidelines.
• Take care of your mouth. Good brushing, flossing, and regular dental visits can help manage gum disease, which may play a role in RA.
• Maintain a healthy weight. Even modest weight loss can reduce inflammatory markers and joint stress.
• Stay active and eat well. A pattern rich in vegetables, fruits, whole grains, lean proteins, and healthy fats supports a less inflammatory environment.
• Monitor symptoms early. If you have risk factors and notice persistent joint pain, stiffness (especially morning stiffness), or swelling, see a rheumatologist promptly.

The goal isn’t perfection; it’s giving your immune system as little reason as possible to spiral into full-blown autoimmunity.

Real-Life Experiences: How Causes and Risk Factors Play Out

Lists of risk factors are helpful, but they can also feel abstractlike reading the weather report for a city you’ve never visited. To make the causes of rheumatoid arthritis feel more down-to-earth, it’s useful to look at how these pieces fit together in real people’s lives. The following examples are composites based on common patterns that rheumatologists see; they’re not any single real person’s story, but they reflect real-world experiences.

Case 1: The “healthy” 32-year-old who never smoked

Emma is 32, a non-smoker, and generally active. When she starts waking up with stiff fingers that take more than an hour to loosen up, she blames her computer job and new workout routine. Her primary-care doctor orders blood work, and it turns out she’s positive for anti-CCP antibodies. A rheumatologist diagnoses early RA.

On paper, Emma doesn’t have the classic cigarette-smoking risk factor. But her mother and aunt both have autoimmune conditions, and later genetic testing shows she carries a high-risk HLA-DRB1 type. Looking back, Emma remembers years of intermittent gum bleeding and delayed trips to the dentist. Her rheumatologist explains that in someone like hergenetically primed for autoimmunitychronic gum inflammation might have helped “wake up” the immune system.

For Emma, understanding the causes of rheumatoid arthritis isn’t about blaming herself; it’s about seeing how genes and environment teamed up quietly over time. It also motivates her to prioritize dental care, stress management, and staying on top of treatment so the disease doesn’t get a head start.

Case 2: The long-time welder and ex-smoker

Luis is 55 and has spent three decades working around dust and fumes in industrial settings. He smoked heavily in his 20s and 30s but quit years ago. When his wrists and knees start aching and swelling, he assumes it’s “just getting older”until he can’t grip his tools without pain.

Testing shows high levels of rheumatoid factor and anti-CCP, along with signs of lung inflammation on imaging. His rheumatologist explains that his past smoking and long-term occupational exposures may have inflamed his lungs enough to trigger RA in a genetic background he never knew he had.

For Luis, learning the likely causes of his RA is bittersweet. He can’t undo decades of exposure, but quitting smoking probably prevented even worse damage. Now, understanding that RA is not just “old age” helps him take treatment seriously and advocate for safer conditions for younger workers coming up behind him.

Case 3: The new mom with sudden joint pain

Maya is 29 and recently had her first baby. During pregnancy, she felt surprisingly goodless joint achiness than usual, more energy. But a few months after delivery, she develops severe morning stiffness in her hands and feet. Some days, just fastening her baby’s onesie feels like a major victory.

Her rheumatologist tells her something many women with RA hear: pregnancy can temporarily dial down autoimmune activity, and the postpartum period can flip that switch back on, sometimes dramatically. Hormonal shifts, sleep deprivation, and the stress of caring for a newborn may all play a role. In Maya’s case, a family history of autoimmune disease plus hormonal changes around childbirth likely set the stage.

For Maya, understanding the hormonal piece of the puzzle is validating. She isn’t “just tired” or “overreacting”; there’s a biological explanation for why RA surfaced when it did. With treatment and support, she learns to manage her symptoms and plan future pregnancies in close partnership with her rheumatology and obstetric teams.

The emotional side of understanding causes

People often want to know the cause of their rheumatoid arthritis for two big reasons: to avoid unnecessary guilt and to regain a sense of control. In reality, RA usually comes from a mix of factors you can’t change (genes, age, many early-life exposures) and factors you can (smoking, gum health, certain occupational risks, weight, stress, and sleep).

Focusing on blame“If only I hadn’t smoked” or “If only I flossed more”doesn’t help your joints. Focusing on agency does. Understanding the causes of RA can help you:

• Take modifiable risk factors seriously (especially quitting smoking and protecting your lungs).
• Catch symptoms early, which gives modern RA medications their best chance to prevent joint damage.
• Explain your disease to friends, family, and employers in a way that makes sense and reduces stigma (“No, this isn’t just wear and tear.”).

You didn’t choose your genes. You probably didn’t choose your childhood environment. And you certainly didn’t choose an immune system that misreads your joint lining as the bad guy. But you can choose how quickly you respond, which lifestyle levers you pull, and how actively you partner with your healthcare team going forward.

That’s the real power of understanding the causes of rheumatoid arthritis: not rewriting the past, but shaping what happens next.