The “Tendon-to-Bone” Problem in Psoriatic Arthritis and Spondyloarthritis: Why Enthesitis Flares, What Actually Helps, and When Biologics Make Sense

Enthesitis means inflammation at an enthesis—the place where a tendon, ligament, or joint capsule anchors into bone. If you have spondyloarthritis or psoriatic arthritis, enthesitis is not a minor side issue; it can be the main driver of pain, stiffness, and loss of function. It is also one reason people are told their “plantar fasciitis” or “tennis elbow” keeps coming back despite rest, insoles, or injections.

What makes enthesitis tricky is that it sits at the intersection of mechanical load (how much stress your tendon insertions take) and immune-driven inflammation (how your immune system misfires in these diseases). That combination explains why symptoms can flare after a long walk, a new workout, weight gain, or even prolonged standing—yet still behave like an inflammatory arthritis problem rather than a simple overuse injury.

Enthesitis commonly affects:

• Heel (Achilles tendon insertion; plantar fascia)
• Bottom of the foot (plantar fascia)
• Elbow (lateral epicondyle area)
• Kneecap region (quadriceps/patellar tendon insertions)
• Hip (greater trochanter region)
• Chest wall (where ribs meet the breastbone, causing costochondral pain)

In psoriatic arthritis, enthesitis often travels with tendon sheath inflammation and whole-finger/toe swelling (dactylitis). In axial spondyloarthritis (a major subtype of spondyloarthritis), enthesitis can coexist with inflammatory back pain and inflammation at spinal/ pelvic ligament attachments. The overall treatment strategy in modern guidelines increasingly emphasizes controlling inflammation early and using targeted therapy when needed.

There is no single cause. Enthesitis happens when genetic risk, immune signaling, and mechanical stress combine in a way that keeps the body’s “repair response” switched on.

The enthesis is not just a simple attachment point. It is a transition zone where soft tissue gradually blends into bone. This region is designed to handle force—but it is also vulnerable to micro-injury and repetitive stress.

When stress is high (standing jobs, running, jumping, new gym routines, obesity, poor footwear, tight calf muscles), the body may respond with repair. In people with spondyloarthritis or psoriatic arthritis, that repair response can be hijacked into chronic inflammation.

In spondyloarthritis and psoriatic arthritis, immune activity involving pathways like tumor necrosis factor, interleukin-17, and interleukin-23 is strongly linked to inflammation at entheses and related structures. This is one reason medications that target these pathways can work when general painkillers do not. Modern treatment recommendations for both psoriatic arthritis and axial spondyloarthritis include these targeted options when disease activity persists.

Many people notice a pattern: symptoms worsen after activity, but rest does not fully solve it—and stiffness is often worse in the morning or after inactivity. That pattern can reflect a mechanoinflammation loop:

• Mechanical load causes micro-stress at the enthesis
• The immune system responds too strongly
• Inflammation increases sensitivity and impairs normal healing
• The enthesis becomes even more reactive to the next round of load

Enthesitis pain is often:

• Very focal (you can point to the spot with one finger)
• Worse with first steps in the morning or after sitting (classic heel enthesitis pattern)
• Worse with pressure (squeezing the heel sides, pressing the tendon insertion)
• Triggered by use, but with an inflammatory quality (stiffness, warmth, swelling)

Common mislabels include:

• Plantar fasciitis
• Achilles tendinopathy
• Tennis elbow
• Trochanteric bursitis (sometimes the pain is actually tendon insertion inflammation nearby)
• Costochondritis (which can be inflammatory in spondyloarthritis, not just mechanical)

• Personal or family history of psoriasis
• Past episodes of red, painful eye inflammation (uveitis)
• History of inflammatory bowel disease
• Inflammatory back pain pattern (better with movement, worse with rest)
• Multiple enthesitis sites at the same time
• Pain that returns quickly when anti-inflammatory medication is stopped

Diagnosis often starts with:

• Targeted tenderness at classic enthesis sites
• Swelling and pain provoked by resisted movement (for example, calf raise aggravating Achilles insertion)
• Looking for the bigger picture: psoriasis, nail changes, dactylitis, inflammatory back pain, uveitis, bowel symptoms.

Some clinicians also use standardized scoring systems in specialist settings (more common in research and rheumatology practices), but in real life, the decision to escalate treatment usually hinges on symptom burden, function, and persistence.

Imaging can help when:

• The site is hard to assess (hip region)
• The diagnosis is uncertain
• Symptoms persist despite reasonable treatment
• The clinician wants to confirm active inflammation before escalating therapy

Ultrasound can show tendon thickening, inflammation around the enthesis, and increased blood flow signals. Magnetic resonance imaging can show deeper inflammation and bone marrow edema near insertions, especially in complex regions.

A good plan usually combines mechanical unloading + anti-inflammatory control + targeted therapy when indicated.

Complete rest often backfires because stiffness increases and surrounding muscles weaken. Instead:

• Temporarily reduce high-impact activity (running, jumping)
• Switch to lower-impact conditioning (cycling, swimming, elliptical if tolerated)
• Avoid sudden spikes in activity (big weekend walks after a sedentary week)

• Supportive shoes with shock absorption
• Heel lifts (short-term) if Achilles insertion is very painful
• Plantar fascia and calf stretching done gently and consistently
• Avoid barefoot walking on hard floors when flaring

A skilled physiotherapist can address:

• Calf tightness and ankle mobility (heel pain)
• Hip abductor weakness (outer hip pain)
• Eccentric loading protocols when appropriate (used carefully in inflammatory states)
• Gait and footwear review

The goal is not just pain relief; it is lowering repeated micro-stress at the insertion.

Non-steroidal anti-inflammatory drugs are commonly used for symptom control, especially in axial spondyloarthritis, and are typically a first-line pharmacologic option. In psoriatic arthritis guidance, they are generally reserved for milder disease and short-term use rather than as a long-term stand-alone strategy.

• If one non-steroidal anti-inflammatory drug does not work, another may
• Risk review matters (blood pressure, kidney function, stomach ulcers, heart disease)

Local corticosteroid injection may help selected sites, especially when a single enthesis is dominating symptoms. However, injections near the Achilles tendon require extra caution due to tendon risk, and repeated injections are generally not a long-term solution.

Medications like methotrexate are commonly used for peripheral joint disease in psoriatic arthritis, but enthesitis often responds less reliably to conventional disease-modifying antirheumatic drugs compared with targeted therapies. Treatment strategies in major recommendations reflect this reality by moving to targeted agents when key domains (like enthesitis) remain active.

If enthesitis is persistent, function-limiting, or part of moderate-to-severe disease, targeted therapy is commonly considered. The main categories include:

Tumor necrosis factor inhibitors are widely used in both psoriatic arthritis and axial spondyloarthritis and have strong evidence across multiple disease domains. They are frequently recommended as an advanced option when conventional approaches fail. They are also often preferred when certain coexisting conditions are present (for example, recurrent uveitis or inflammatory bowel disease, depending on the specific agent).

Interleukin-17 inhibitors can be highly effective for psoriatic disease domains (skin and joints) and are included as advanced therapy options in axial spondyloarthritis recommendations as well.

Important caution: interleukin-17 inhibitors are generally not started in active inflammatory bowel disease because they may worsen intestinal inflammation; multiple guidelines and reviews highlight this concern.

These agents are prominent in psoriatic arthritis treatment discussions and recommendations, particularly when skin disease is significant. They are part of the broader targeted strategy described in updated psoriatic arthritis recommendations.

(For axial disease specifically, some interleukin-23 approaches have not shown the same consistent benefit, which is why medication choice often depends on whether the dominant problem is axial symptoms, peripheral arthritis, skin disease, or enthesitis.)

Janus kinase inhibitors are included among advanced therapy options in axial spondyloarthritis recommendations when disease activity remains high despite conventional measures. They can also be used in psoriatic arthritis strategies depending on prior treatment response, comorbidities, and risk factors.

Biologics are usually considered when enthesitis is not just annoying, but clinically meaningful—persistent, inflammatory, and limiting function despite appropriate first steps.

A rheumatology team may consider biologics when:

1. Enthesitis persists despite adequate trials of non-steroidal anti-inflammatory drugs and a structured rehab plan
2. Pain is function-limiting (walking, working, sleep, climbing stairs)
3. There are multiple enthesitis sites or recurrence is frequent
4. Enthesitis is part of broader active disease (peripheral joints, inflammatory back pain, dactylitis, significant psoriasis)
5. Imaging supports active inflammation and not only degenerative change
6. There is high overall disease activity and the goal is to prevent ongoing damage and disability, consistent with modern strategy-based recommendations

Psoriatic arthritis is often treated with a “domain-based” approach: what is driving disability right now—peripheral joints, skin, enthesitis, dactylitis, spine, nails? Enthesitis is considered a major domain, and evidence reviews specifically addressing enthesitis management emphasize that targeted therapies and certain nonpharmacologic measures are central when enthesitis is prominent.

Selection is not just about “strongest medication.” It is about matching therapy to the whole patient:

• If inflammatory bowel disease is active, clinicians often avoid starting interleukin-17 inhibitors.
• If psoriasis is severe, interleukin-17 or interleukin-23 pathway options may be appealing.
• If recurrent uveitis is a major issue, certain tumor necrosis factor monoclonal antibodies are often preferred in guidance discussions.

• Track patterns: morning stiffness, response to non-steroidal anti-inflammatory drugs, flare triggers
• Treat mechanical contributors: footwear, calf flexibility, hip strength
• Address weight and smoking (both can worsen inflammatory burden and load)
• See a rheumatologist early if multiple sites or psoriasis + heel pain appear together

• Assume every heel/elbow pain is purely mechanical if you have psoriasis or inflammatory back pain
• Repeatedly inject the same site without a long-term inflammatory control strategy
• “Push through” high-impact training during a flare (this often prolongs it)

Seek prompt medical evaluation if you have:

• Fever, chills, or a hot swollen area suggesting infection
• Sudden inability to push off the foot or a “snap” sensation (possible tendon rupture)
• Rapidly worsening pain with marked swelling and redness
• Chest pain that could be cardiac (do not assume it is chest-wall enthesitis)
• New neurologic symptoms (weakness, bowel/bladder changes) with back pain

• Enthesitis is inflammation where tendons and ligaments attach to bone and is a hallmark pain generator in spondyloarthritis and psoriatic arthritis.
• It often behaves like a hybrid problem: mechanical stress triggers it, but immune inflammation sustains it.
• First-line care typically includes load management, physiotherapy, supportive footwear/orthotics for heel disease, and anti-inflammatory medication when appropriate.
• If enthesitis is persistent or disabling, modern treatment strategies commonly move to targeted therapies such as tumor necrosis factor inhibitors, interleukin-17 inhibitors, interleukin-23 pathway agents, or Janus kinase inhibitors—chosen based on the dominant disease domains and comorbidities.
• Biologics are typically considered when symptoms remain active despite initial measures or when enthesitis is part of broader moderate-to-severe disease.

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