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8.26.19 7:06AM

Tina Donvito

Home Living with Arthritis Symptoms

What Is Enthesitis? The Painful Arthritis Symptom You Should Know About

PUBLISHED 08/26/19 BY Tina Donvito

Certain types of arthritis are prone to pain where tendons and ligaments meet bone, which is called enthesitis. Here’s how to deal with it.

If you have ankylosing spondylitis or psoriatic arthritis , you may be familiar with the pain of enthesitis, an inflammation where tendons and ligaments attach to the bone — even if you aren’t aware it has a name. “I didn’t know what it was called!” Monica D. told us on Facebook. “I have pain all the time. Makes it difficult to walk very far.”

What Is Enthesitis?

“Enthesitis is inflammation of the ‘enthesis,’ which is where a tendon or ligament attaches to bone,” says Joan Appleyard, MD, a rheumatologist at Baylor College of Medicine in Houston, Texas. “Symptoms are pain sometimes accompanied by swelling.”

There’s a reason the enthesis is susceptible to this problem. “The enthesis has a lot of blood flow and [thus] is subject to both infection and inflammation,” says Theodore R. Fields, MD, a professor of clinical medicine at Weill Cornell Medical College and an attending rheumatologist at Hospital for Special Surgery in New York City. “Two of the most common entheses are the area where the Achilles’ tendon inserts on the back of the heel, which causes Achilles’ tendonitis, and where the sheet of connective tissue, or fascia, inserts on the bottom of the heel, which causes plantar fasciitis.”

Types of Arthritis That Cause Enthesitis

If you have rheumatoid arthritis or osteoarthritis, chances are you won’t experience enthesitis, because it generally only occurs with certain types of arthritis called spondyloarthropathies (SpA), which include non-radiographic axial spondyloarthritis, ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis (a type that occurs in people with inflammatory bowel disease), and reactive arthritis (which can occur after infection, formerly called Reiter’s syndrome).

Enthesitis is actually one of the hallmark traits of SpA. “It is not a feature of rheumatoid arthritis — this is one of the ways in which SpA differs from RA,” Dr. Appleyard says.

Doctors aren’t exactly sure why SpA targets the enthesis, but it may be that a specific inflammatory response occurs in areas under biomechanical stress (stress on the joint from movement).

“About half of people with psoriatic arthritis and ankylosing spondylitis have enthesitis,” says Dr. Fields. “In both psoriatic arthritis and ankylosing spondylitis, the back and under portions of the heel are common sites of enthesitis.”

There are many other areas where enthesitis can occur, he says, including the inner and outer sides of the elbows, the area where the ribs meet the breastbone , the back of the head where it meets the neck, and in the spine in the area closest to the skin.

What Does Enthesitis Feel Like?

The main symptom of enthesis is pain, which CreakyJoints patients described as “horrible” or “burning.”

“Quite a bit of my PsA pain is due to enthesitis,” Ruth O. shared on Facebook. “It moves around from ball of my foot, to left shoulder, hands, wrists and left hip.”

Marcia G. told us, “I have [enthesitis] in my right ankle and heel mostly. My feet hurt randomly and the right toes and top of foot swell up.” Although many patients noted that enthesitis occurs in their feet, Kelly C. says it hurts “especially around my rib cage.”

Does Enthesitis Signal Worsening Disease?

Enthesitis might not mean your disease is progressing. “Enthesitis can be part of both severe and relatively mild cases of psoriatic arthritis or ankylosing spondylitis,” Dr. Fields says. It may indicate active disease, but not necessarily worsening disease, says Dr. Appleyard.

Your doctor will diagnose enthesitis based on a physical exam, in which they’ll note the location of pain, tenderness, or swelling. “Ultrasound can also be helpful in diagnosing enthesitis, and at times MRI can also be used,” Dr. Fields says.

Treatment for Enthesitis

“Managing enthesitis is important since it can cause a lot of discomfort,” Dr. Fields says. Some specific biologic therapies used to treat SpA seem to improve symptoms of enthesitis. “Treating the underlying disease with anti-TNF agents [a type of biologic] often helps with enthesitis, but traditional DMARDs such as sulfasalazine don’t treat enthesitis,” Dr. Appleyard says. Non-steroidal anti-inflammatory agents (NSAIDs) can be used for mild cases.

When deciding on a treatment regimen for SpA, Dr. Fields says it’s important to take into account all the affected areas. “In patients where enthesitis is the major issue, and more severe than the arthritis, we may skip the non-biologic agents and go directly to biologic therapies, since they tend to be more effective for enthesitis,” he says.

In addition to TNF blockers, other biologic options include blockers of the proteins IL-17, IL-12, or IL-23. “One exception is the non-biologic agent apremilast, which does not appear to cause infection and can be used in psoriatic arthritis, and which has been shown to have effectiveness in some people with enthesitis,” says Dr. Fields.

In addition, “local injection of corticosteroids can be used in enthesitis at times, but needs to be used carefully to avoid weakening of the surrounding tendons and ligaments,” Dr. Fields says.

Talk to your doctor about which medications are right for your individual case. (Here’s what one study found about picking the right treatment for enthesitis in PsA .)

Home Remedies for Enthesitis

A physical therapist can give you gentle stretches to do at home to help relieve the pain of enthesitis, Dr. Fields says. In addition, the doctors and patients we talked to suggested:

• Apply heat or ice to affected areas
• Maintain a healthy weight. “Weight loss can take pressure off the involved areas,” Dr. Fields says.
• Rest and elevate the affected foot. “I try to keep the swelling down by icing it, and keeping my leg and foot elevated,” Lesley P. told us on Facebook.
• Wear special shoes. “People with plantar fasciitis can benefit from shoe inserts to cushion the heel and may be helped by a consultation with a podiatrist ,” Dr. Fields says.
• Wear compression socks, braces, wraps, or even a medical boot.
• Watch salt intake to control swelling. “Salt intake does make a difference,” Ruth says.
• Over-the-counter remedies (check with your doctor first). “I love using Biofreeze on the bone in my foot — it helps!” Caroline P. told us on Facebook. Other CreakyJoints members recommended Epsom salt soaks, diclofenac gel, magnesium, or CBD products .

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• This Woman’s Misdiagnosed Plantar Fasciitis Foot Pain Was Actually Psoriatic Arthritis
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• Was This Helpful?

Tags: Ankylosing Spondylitis , Psoriatic Arthritis

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Enthesitis and Enthesopathy Explained

A Primary Feature of Spondyloarthritis

If you have seen the words entheses, enthesitis, or enthesopathy in your X-ray or medical reports, the terminology may have been unfamiliar to you. Let's look at the meaning and also how it relates to various types of arthritis and rheumatic diseases.

• Enthesis (plural: entheses) typically refers to the connective tissue where tendons , ligaments, or joint capsules attach to bone. Two types of entheses exist: fibrous entheses and fibrocartilaginous entheses. While that is the classic definition, a newer, broader definition suggests that enthesis is more than a simple attachment or insertion site—enthesis functions as a unit which includes adjacent tissues (for example, bone and fibrocartilage connected to synovium). The unit is referred to as the "enthesis organ complex".
• Enthesopathy is any abnormal condition that affects the entheses (e.g., inflammation of the entheses). Enthesopathy may be due to an inflammatory condition, such as psoriatic arthritis , or a condition related to injury or overload, such as plantar fasciitis.
• Enthesitis refers to inflammation of the entheses.

Enthesitis is typically associated with pain, stiffness, and tenderness at the insertion site, sometimes without much swelling. However, where there is involvement of the large insertions of lower limbs, swelling can be significant and prominent. If swelling is absent, enthesitis can be difficult to recognize or suspect during a physical examination.

Enthesitis is common at the following sites:

• Achilles tendon
• Patellar tendon
• Plantar fascia
• Elbow epicondyles
• Iliac crest

Conditions Associated With Enthesitis

Enthesitis may be linked to inflammatory conditions or it may be mechanically induced by injury. Peripheral enthesitis is characteristic of all of the spondyloarthropathies , including undifferentiated spondyloarthritis, ankylosing spondylitis , psoriatic arthritis, enteropathic arthritis, and reactive arthritis .

Reactive arthritis is a form of arthritis that results from infection. The swelling of reactive arthritis is often triggered by infection in a more remote body part, such as the urinary tract, intestines or genitals. Typically the joints of the knees, feet, and ankles are targets for inflammation secondary to reactive arthritis. More specifically, enthesitis in people with reactive arthritis usually occurs in the plantar fascia, pelvic bones or Achilles tendon. Reactive arthritis is actually uncommon and usually goes away in most people within a year after onset.

Ankylosing spondylitis is an inflammatory condition that is most prevalent in men. The inflammation of ankylosing spondylitis affects the vertebrae and causes them to fuse. Chronic enthesitis of the tendons and ligaments of the vertebrae is the first step in the eventual fusion of vertebrae, which is the main feature of ankylosing spondylitis. People with ankylosing spondylitis can also experience enthesitis of the costochondral joints , or joints of the ribs.

Other conditions associated with enthesitis include Achilles tendinitis, rheumatoid arthritis , osteoarthritis , and diffuse idiopathic skeletal hyperostosis (DISH). It may be degenerative enthesopathy that develops with osteoarthritis. The degenerative changes that occur with wear-and-tear osteoarthritis also affect the fibrocartilages.

Imaging for Diagnosis

Imaging can help diagnose enthesitis, but the imaging modality utilized depends on whether the axial or peripheral skeleton is affected. MRI is used for the axial skeleton. Ultrasound is preferred for the peripheral skeleton. MRI would again be preferable for any insertions that are inaccessible.

Treatment of enthesitis is based on the underlying condition. For example, if enthesitis is due to an inflammatory condition, treatment usually focuses on treating the inflammatory polyarthritis. Treatment, in such cases, may include:

• nonsteroidal anti-inflammatory drugs (NSAIDs)
• methotrexate
• TNF blockers
• Physical therapy

Depending on which areas are involved, local corticosteroid injections may be used if oral medications are inadequate. However, a healthcare provider would almost never use these injections for Achilles tendinitis or into the patella; this could lead to rupture.

The biomechanical aspects of enthesitis are also addressed by using insoles and cushions.

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By Carol Eustice Carol Eustice is a writer covering arthritis and chronic illness, who herself has been diagnosed with both rheumatoid arthritis and osteoarthritis.

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Enthesopathy and Enthesitis

Tendons are the tissues that attach your muscles to your bones. Ligaments are what attach your bones to one another. The place where a tendon or ligament meets your bone is called an enthesis. Your doctor might use the plural, entheses.

Enthesopathy is an umbrella term for conditions that affect these connection points. Enthesitis is when they get inflamed and become painful because of injury, overuse, or disease.

Enthesitis is common in some forms of arthritis , including psoriatic arthritis and ankylosing spondylitis . It also can happen in some children with juvenile idiopathic arthritis (also known as juvenile rheumatoid arthritis ).

It isn’t usually linked to osteoarthritis or adult rheumatoid arthritis (RA), but people with those conditions can have it.

Enthesitis Symptoms

Common spots for enthesitis to happen are around your heel, knee , hip, toe, elbow , backbone, and the bottom of your foot . The inflammation can lead to pain and stiffness, especially when you're moving. You also might notice swelling around those areas.

Soreness at the back of your heel caused by enthesitis is sometimes called Achilles tendinitis or plantar fasciitis pain at the bottom of your foot. This pain can make it hard for you to run or climb stairs.

Over time, enthesitis can lead to:

• Calcification or ossification: Inflammation of the entheses can cause new bone tissue to form. That new bone tissue gets in the way of normal movement and function -- like a bone spur on your heel.
• Fibrosis: Tissues in the affected area become ropey.

Enthesitis Diagnosis

Enthesitis is hard to diagnose. The doctor will give you a physical exam , check for swelling, and to see if the area hurts when compressed. They’ll ask if the pain gets better after you exercise . You might get lab tests that look for signs of inflammation and imaging tests so your doctor can get a good view of your joints.

Enthesitis Treatment

There’s no specific treatment for enthesopathy, but there are treatments for the diseases that lead to it. Usually they’re a mix of exercise , rest, and medication . Your doctor can help you decide what’s right for you. Non-steroidal anti-inflammatory drugs ( NSAIDs ), like naproxen and ibuprofen , can help with inflammation and pain. If the enthesitis is caused by an autoimmune arthritis, your doctor also may prescribe a disease-modifying anti- rheumatic drug (DMARD) or biologics.

They may recommend steroids for areas that are especially stiff or painful.

Types of Enthesopathies

There are many. Some of the most common are:

• Ankylosing spondylitis
• Plantar fasciitis
• Achilles tendinitis
• Rotator cuff syndrome of shoulder and allied disorders
• Enthesopathy of elbow region
• Enthesopathy of wrist and carpus
• Bursitis of hand or wrist
• Enthesopathy of hip region
• Bursitis of hip
• Enthesopathy of knee
• Enthesopathy of ankle , tarsus, and calcaneus

The Connection With Arthritis

Some kinds of arthritis are autoimmune disorders. This means your body's immune system makes chemicals that attack and damage your own tissues. This can cause enthesitis.

It's a common symptom of two kinds of autoimmune arthritis -- psoriatic arthritis and ankylosing spondylitis. Psoriatic arthritis, which is common in people with the skin condition psoriasis , can affect your entire body. Ankylosing spondylitis mainly affects your spine .

Enthesitis also happens in about 10% to 20% of children with juvenile idiopathic arthritis, which can affect one or more joints and lasts at least 6 weeks. These children are described as having enthesitis-related arthritis (ERA).

Kids with juvenile arthritis often have a family history of inflammatory conditions, like ankylosing spondylitis, psoriatic arthritis, or inflammatory bowel disease . They also have eye redness and pain due to inflammation, along with other arthritis symptoms.

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• Review Article
• Published: 21 November 2017

Enthesitis: from pathophysiology to treatment

• Georg Schett 1 ,
• Rik J. Lories 2 ,
• Maria-Antonietta D'Agostino 3 ,
• Dirk Elewaut 4 ,
• Bruce Kirkham 5 ,
• Enrique R. Soriano 6 &
• Dennis McGonagle 7  

Nature Reviews Rheumatology volume  13 ,  pages 731–741 ( 2017 ) Cite this article

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• Immunopathogenesis
• Medical imaging
• Spondyloarthritis

Entheses are predominantly extra-articularly localized structures that represent a key target of musculoskeletal inflammation in diseases such as psoriatic arthritis (PsA) and spondyloarthritis (SpA)

Entheses contain a specific immune microenvironment, which is activated by a combination of factors that include mechanical stress, genetic susceptibility and microbial-triggered immune activation

Enthesitis arises from robust activation of prostaglandin E2 and the IL-23–IL-17 axis, leading to the influx of innate immune cells and homing of inflammation into the entheses, which is followed by mesenchymal tissue responses and new bone formation

Clinical and imaging instruments have been developed that enable the reliable detection and monitoring of enthesitis in patients with PsA and SpA

Inhibition of the key effector cytokines of enthesitis — IL-17, IL-23 and TNF — has shown to be effective in supporting the resolution of enthesitis in PsA and SpA

Entheses are the insertion sites of tendons and ligaments to the bone surface and are essential structures for locomotion. Inflammation of the entheses (enthesitis) is a key feature of psoriatic arthritis and spondyloarthritis. To date, our conceptual understanding of enthesitis remains limited. This Review provides an insight into the pathophysiology of enthesitis, addressing the role of biomechanics, prostaglandin E2-mediated vasodilation and the activation of innate immune cells in the initiation phase of enthesitis, as well as the role of entheseal IL-23-responsive cells that augment inflammation by producing pro-inflammatory mediators such as IL-17A, IL-22 and TNF. In addition, the molecular steps that translate inflammation into resident tissue responses, resulting in new bone formation, are discussed. The second part of the article summarizes the clinical features of enthesitis, and the role of clinical and imaging instruments in detecting enthesitis are discussed together with their challenges and limitations. Finally, the Review summarizes the current treatment possibilities for enthesitis based on the aforementioned pathophysiological concepts, focusing on the role of cytokine-blocking agents.

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Acknowledgements

This work is supported by the Collaborative Research Center (CRC) 1181 of the German Research Council (Deutsche Forschungsgemeinschaft-DFG). D.M.'s work is funded by the Leeds NIHR Biomedical Research Centre.

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Schett, G., Lories, R., D'Agostino, MA. et al. Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol 13 , 731–741 (2017). https://doi.org/10.1038/nrrheum.2017.188

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arthritis health center / arthritis a-z list / enthesitis and enthesopathy article

Enthesitis and Enthesopathy

• Medical Author: William C. Shiel Jr., MD, FACP, FACR
• Medical Author: Karthik Kumar, MBBS
• Medical Editor: Melissa Conrad Stöppler, MD

What are enthesitis and enthesopathy?

What causes enthesitis and enthesopathy, what are the symptoms of enthesitis and enthesopathy, diagnosis of enthesitis and enthesopathy, what is the treatment for enthesitis and enthesopathy, what medications are used for enthesopathy, what is the prognosis of enthesitis and enthesopathy, is it possible to prevent enthesitis and enthesopathy, frequently asked questions.

Enthesopathy is a general term that refers to a disorder affecting the site where tendons, ligaments, or other soft tissues attach to bone, known as the enthesis. Enthesitis, on the other hand, is a specific type of enthesopathy that refers to inflammation of the entheses.

Types of enthesopathy

Enthesopathy is named by the location in the body where it occurs.

• Spinal ankylosing spondylitis is a typical example where inflammation at the entheses causes pain and stiffness in the spine.
• Diffuse idiopathic skeletal hyperostosis (DISH): A condition characterized by the calcification and ossification of ligaments and entheses, leading to stiffness and pain in the spine.

Spinal enthesopathy can lead to the formation of new bone at the entheses, known as syndesmophytes. Over time, these can cause the spine to fuse, which is a characteristic feature of ankylosing spondylitis.

Calcaneal enthesopathy: Calcaneal enthesopathy affects the entheses at the heel bone (calcaneus). Key conditions include:

• Plantar fasciitis : Inflammation at the insertion of the plantar fascia into the calcaneus, causing heel pain .
• Achilles tendon enthesopathy: Inflammation or degeneration at the insertion of the Achilles tendon into the calcaneus. It can lead to pain, swelling, and limited movement in the heel. Chronic stress or repetitive use is often a contributing factor.

Enthesopathy calcaneus:

• This condition specifically refers to enthesopathy at the heel bone. It includes both inflammatory and degenerative changes at the insertion of tendons or ligaments into the calcaneus.
• Overuse, trauma , and systemic inflammatory conditions such as rheumatoid arthritis or psoriatic arthritis can contribute to this disorder.

Achilles tendon enthesopathy:

• This is a type of calcaneal enthesopathy involving the Achilles tendon. It is characterized by pain at the back of the heel, particularly during or after physical activity.
• It can be associated with systemic conditions such as spondyloarthropathies or result from overuse injuries.

Enthesopathy of the knee: Knee enthesopathy affects the entheses around the knee joint . It can involve several structures:

• Patellar tendon: Inflammation or degeneration at the insertion of the patellar tendon into the tibia (tibial tuberosity), commonly seen in conditions such as Osgood-Schlatter disease .
• Quadriceps tendon: Enthesopathy at the insertion of the quadriceps tendon into the patella can lead to pain and dysfunction in the knee joint.

Pelvic enthesopathy: Pelvic enthesopathy involves the entheses around the pelvis, including:

• Ischial tuberosity: This is where the hamstring muscles attach. Enthesopathy here can cause buttock pain, particularly worsened by sitting.
• Iliac crest: This site serves as the insertion point for abdominal and gluteal muscles. Enthesopathy at this location can lead to pain in the pelvis and lower back.

Pelvic enthesopathy is often associated with systemic inflammatory conditions such as ankylosing spondylitis or psoriatic arthritis , where inflammation at the pelvic entheses contributes to overall disease pathology.

Enthesopathy can be caused by injury or diseases. When it affects a single area of the body, it is often due to injury. Conversely, when it affects multiple areas, underlying disorders are more likely to be the cause.

There are several potential causes of enthesitis and enthesopathy, which can be broadly categorized into the following:

Inflammatory arthritides

• Ankylosing spondylitis: A chronic inflammatory disease primarily affecting the spine and sacroiliac joints. Enthesitis is a hallmark of this condition, often seen at the Achilles tendon and plantar fascia.
• strong>Psoriatic arthritis: An inflammatory arthritis associated with psoriasis . Enthesitis is common, particularly at the Achilles tendon, plantar fascia, and around the elbow.
• Reactive arthritis : Follows an infection (often gastrointestinal or genitourinary). Enthesitis often involves the lower limbs, especially the Achilles tendon.
• inflammatory bowel disease ( IBD )-related arthritis: Conditions such as Crohn's disease and ulcerative colitis can be associated with enthesitis, typically affecting the lower limbs.

Degenerative conditions

• Osteoarthritis : Degenerative changes in joints can extend to the entheses, causing secondary enthesopathy due to altered biomechanics and increased stress on the attachment sites.

Mechanical stress and overuse

• Repetitive strain injury: Chronic overuse of a joint can lead to microtrauma at the enthesis, causing inflammation. This is common in athletes and individuals with occupations requiring repetitive movements.
• Obesity : Excessive weight can increase mechanical stress on weight-bearing entheses, particularly at the knees and feet .
• Acute injury: Direct trauma or injury to an enthesis can lead to inflammation and subsequent enthesitis. Common sites include the Achilles tendon and elbow.
• Chronic microtrauma: Repeated minor injuries can accumulate over time, leading to enthesopathy.

Metabolic and endocrine disorders

• Diabetes mellitus : Poor blood glucose control can lead to abnormal collagen formation and calcification at the entheses, causing pain and inflammation.
• Gout : Uric acid crystal deposition can occur in the entheses, causing inflammation and pain, typically at the Achilles tendon or knees.

Infectious causes

• Direct infection: Bacterial or viral infections can directly infect the entheses, though this is rare. An example is reactive arthritis after a Chlamydia or Salmonella infection .
• Tuberculosis : In rare cases, Mycobacterium tuberculosis can infect the entheses, leading to chronic inflammation.

Genetic factors

• HLA-B27: This genetic marker is strongly associated with ankylosing spondylitis and other spondyloarthropathies, which often present with enthesitis.
• Family history: A family history of spondyloarthropathies or other inflammatory arthritides can increase the risk of developing enthesitis.
• Autoimmune diseases: Autoimmune diseases like psoriatic arthritis, reactive arthritis, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis (DISH), and rheumatoid arthritis can cause enthesitis as the immune system attacks tissues within the joints.

Medications

• Fluoroquinolones: Antibiotics in this class can cause tendinitis and enthesitis, particularly affecting the Achilles tendon.
• Steroid use: Long-term steroid use can lead to tendon weakening and increased susceptibility to enthesitis.

Other systemic diseases

• Sarcoidosis : This inflammatory disease can involve the entheses, leading to granulomatous inflammation and pain.
• Systemic lupus erythematosus ( SLE ): Although less common, SLE can cause enthesitis as part of its widespread inflammatory effects on connective tissue.
• Age-related changes: Degenerative changes and reduced elasticity in tendons and ligaments with aging can predispose individuals to enthesitis.

Understanding the specific cause of enthesitis or enthesopathy is crucial for targeted treatment and management, as the underlying condition often dictates the therapeutic approach.

Enthesitis and enthesopathy can have similar symptoms because they both involve inflammation or structural changes at the entheses (the sites where tendons and ligaments attach to bone).

Common symptoms

• Pain: Pain is a common symptom of enthesitis and enthesopathy. It can range from mild to severe and is often described as a burning or intense pain in the affected area.
• Stiffness: Stiffness is another common symptom, which can make it difficult to move the affected joint or area.
• Swelling: Swelling is often present in the affected area, which can be accompanied by redness and warmth.
• Tenderness: Tenderness is another common symptom, especially when pressure is applied to the affected area.

Specific symptoms

• Achilles tendinitis: Pain in the back of the heel, which can make it difficult to run or climb stairs.
• Plantar fasciitis: Pain in the bottom of the foot, which can make it difficult to walk or stand.
• Rotator cuff syndrome: Pain in the shoulder, which can make it difficult to lift or rotate the arm.
• Bursitis : Pain and swelling in the joints, which can make it difficult to move the affected joint.
• Fibrosis: Thickening and scarring of soft body tissues, which can lead to permanent changes in the affected area.
• Calcification or ossification: Formation of new bone tissue, which can lead to bone spurs and permanent changes in the affected area.

Other signs and symptoms

• Nail changes: Changes in the fingernails or toenails, such as nail cracking, pitting, or separation from the nail bed.
• Dactylitis: Inflammation of the fingers or toes, which can be painful and make it difficult to move the affected digit.
• Fatigue : Fatigue is a common symptom, especially in individuals with chronic enthesitis.

These symptoms can vary in severity depending on the underlying cause and the extent of inflammation or damage at the enthesis. It's essential to consult a health care professional for an accurate diagnosis and appropriate management.

Enthesitis is usually diagnosed clinically by simple examination by a health care professional. Radiologic testing can sometimes demonstrate calcification or spur formation in the area if the enthesitis is chronic. MRI scanning can highlight inflamed tissues.

Enthesitis and enthesopathy are clinically diagnosed when the following three criteria are met

• Current or recent (within the past two weeks) pain
• Local tenderness
• Pain on resisted motion or traction

Diagnosing enthesitis involves a combination of clinical evaluation, imaging studies, and sometimes laboratory tests.

Clinical evaluation:

• History and physical examination: The doctor will take a detailed medical history and ask about symptoms such as pain, swelling, and stiffness, especially at tendon or ligament attachment sites. Common sites include the Achilles tendon, plantar fascia, and lateral epicondyle.
• Palpation: Tenderness at the enthesis is a key clinical finding. The physician will palpate the entheses to check for pain and swelling.

Imaging studies:

• Ultrasound : This is a sensitive tool for detecting early changes in enthesitis. It can show thickening of the enthesis, erosions, calcifications, and increased blood flow (indicating inflammation).
• Magnetic resonance imaging (MRI): It is useful for visualizing both soft tissue and bone involvement. It can detect bone marrow edema , which is indicative of active inflammation at the enthesis.
• X-rays : While less sensitive to early changes, X-rays can show bone changes such as erosions or new bone formation at the enthesis in chronic cases.

Laboratory tests:

• Inflammatory markers: Blood tests for markers of inflammation, such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), may be elevated in cases of enthesitis, although they are not specific.
• HLA-B27: Testing for the HLA-B27 gene can be helpful, particularly if a spondyloarthropathy (a group of inflammatory rheumatic diseases that involve the entheses) is suspected.

Diagnosis of enthesopathy:

• History and physical examination: Similar to enthesitis, the physician will take a detailed history and perform a physical exam to identify symptoms such as pain, swelling, and functional limitations at the entheses.
• Palpation: The doctor will palpate the affected entheses to identify tenderness and any abnormal changes.
• Ultrasound: This can help differentiate between inflammatory and degenerative changes at the enthesis. Ultrasound may show changes such as thickening, calcification, or tears in the tendon or ligament.
• MRI: MRI is particularly useful for distinguishing between different types of enthesopathies. It can show detailed images of soft tissue and bone, including inflammation, edema, and degenerative changes.
• X-rays: X-rays can reveal chronic changes such as calcification, bone spurs, or erosions. They are less useful for detecting early or purely soft tissue changes.
• Inflammatory markers: In cases of inflammatory enthesopathy (such as enthesitis), markers such as CRP and ESR might be elevated.
• Rheumatologic tests: If a systemic inflammatory disease is suspected, additional tests such as rheumatoid factor (RF) or anti-cyclic citrullinated peptide (anti-CCP) antibodies may be performed.

Enthesitis and enthesopathy are diagnosed primarily through clinical history and examination, with imaging and laboratory tests used to support the diagnosis and identify underlying causes. A combination of these modalities is often required for an accurate diagnosis.

Enthesitis is treated by measures that decrease inflammation and pain. This includes rest from activity, cold application, and anti-inflammatory medications. Physical therapy is sometimes incorporated as part of the treatment regimen.

The main treatment options for enthesitis and enthesopathy include:

• Nonsteroidal anti-inflammatory drugs ( NSAIDs ): NSAIDs such as ibuprofen , naproxen , and diclofenac are often the first-line treatment for enthesitis. They can help reduce inflammation and pain at the enthesis.
• Corticosteroid injections: Local corticosteroid injections into the affected enthesis can provide rapid relief of pain and inflammation. However, the benefits may be short-term, and repeated injections can lead to side effects such as tendon weakening.
• Disease-modifying antirheumatic drugs (DMARDs): For patients with underlying inflammatory conditions such as psoriatic arthritis or ankylosing spondylitis, DMARDs such as methotrexate , sulfasalazine , and leflunomide can help manage the underlying disease and reduce enthesitis.
• Biologic therapies: Newer biologic drugs that target specific inflammatory pathways, such as TNF-alpha inhibitors (such as adalimumab , etanercept ), IL-17 inhibitors (such as secukinumab, ixekizumab), and IL-23 inhibitors (such as ustekinumab ), have shown efficacy in treating enthesitis associated with conditions such as psoriatic arthritis and ankylosing spondylitis.
• Physical therapy: Stretching, strengthening exercises, and other physical therapy modalities can help improve mobility and function in patients with enthesitis. This can include techniques such as ultrasound, laser therapy, and extracorporeal shock wave therapy.
• Lifestyle modifications: For overuse or injury-related enthesopathies, rest, ice, compression, and elevation (RICE) can help manage acute symptoms. Avoiding or modifying activities that aggravate the condition is also important.
• Surgical treatment: In rare, severe, or treatment-resistant cases, surgical procedures such as tendon release or entheseal debridement may be considered, but these are generally reserved as a last resort.

Each of these treatment options can be used alone or in combination, depending on the severity of the condition, patient preferences, and response to treatment. A multidisciplinary approach often yields the best results, involving rheumatologists , physical therapists, orthopedic surgeons, and other health care professionals.

The medications used to treat enthesopathy aim to reduce pain and inflammation, as well as improve function. Here are the main categories of medications used for enthesopathy:

Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs are commonly used to relieve pain and reduce inflammation in patients with enthesopathy.

• Ibuprofen ( Advil , Motrin )
• Naproxen ( Aleve )
• Diclofenac ( Voltaren )
• Celecoxib ( Celebrex )

Mechanism of action: NSAIDs work by inhibiting cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins that cause inflammation and pain.

Analgesics: These medications are used primarily for pain relief and do not have significant anti-inflammatory effects.

• Acetaminophen ( Tylenol )

Mechanism of action: Analgesics work by blocking pain signals in the nervous system or by acting on certain receptors to decrease the perception of pain.

Corticosteroids : Corticosteroids are potent anti-inflammatory medications that can be used for severe inflammation.

• Methylprednisolone ( Medrol )
• Dexamethasone

Mechanism of action: Corticosteroids mimic the effects of cortisol, a hormone produced by the adrenal glands, to reduce inflammation by suppressing the immune response.

Disease-modifying antirheumatic drugs (DMARDs): DMARDs are used particularly in cases where enthesopathy is related to inflammatory diseases such as ankylosing spondylitis or psoriatic arthritis.

• Methotrexate
• Sulfasalazine
• Leflunomide

Mechanism of action: DMARDs work by modifying the immune system to slow down the progression of the disease and decrease inflammation.

Biologic DMARDs: These are a newer class of DMARDs that target specific components of the immune system.

• Tumor necrosis factor (TNF) inhibitors: Etanercept ( Enbrel ), Infliximab ( Remicade ), Adalimumab ( Humira )
• Interleukin inhibitors: Secukinumab (Cosentyx), Ustekinumab ( Stelara )

Mechanism of action: Biologics work by targeting specific molecules involved in the inflammatory process, such as TNF-alpha or interleukins, to reduce inflammation and prevent joint damage.

Local injections: For localized pain and inflammation, injecting corticosteroids directly into the affected area can provide relief.

• Triamcinolone
• Methylprednisolone

Mechanism of action: These injections deliver a high dose of corticosteroids directly to the site of inflammation, reducing local inflammation and pain.

These medications and treatments are often used in combination, depending on the severity of the condition and the underlying cause. It's essential to consult with a health care provider to determine the most appropriate treatment plan.

Platelet-rich plasma (PRP): PRP injections, which use concentrated platelets from the patient's own blood, are being investigated as a treatment to promote healing of the entheses. The growth factors in platelets may stimulate tissue repair, but more research is needed on their efficacy.

NSAIDs are the mainstay of treatment, with corticosteroid injections used for severe cases. DMARDs and biologics are used if enthesopathy is caused by inflammatory arthritis. Other adjunct therapies such as topical nitrates and PRP injections may also be tried in some cases.

The prognosis of enthesitis and enthesopathy can vary depending on the underlying cause, severity, and the patient's overall health.

• Chronic condition: Enthesitis is often a chronic condition, especially when associated with systemic inflammatory diseases. The prognosis depends largely on the management of the underlying disease.
• Treatment response: With appropriate treatment, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), and biologics (such as TNF inhibitors), many patients can achieve good symptom control and improved quality of life.
• Complications: Without effective treatment, enthesitis can lead to significant pain, stiffness, and reduced mobility. Over time, chronic inflammation can cause structural damage and contribute to joint deformities and functional impairment.
• Individual variation: The course of the disease can vary widely among individuals. Some patients experience episodic flares with periods of remission, while others may have persistent symptoms.

Enthesopathy

• Variable outcomes: The prognosis of enthesopathy varies depending on the specific condition and its cause. Non-inflammatory enthesopathies, such as tendinopathies, often have a better prognosis than inflammatory enthesopathies.
• Response to treatment: Effective management typically involves a combination of rest, physical therapy, pain management (NSAIDs, corticosteroid injections), and addressing any underlying causes (such as biomechanical issues or systemic diseases). Patients often experience significant symptom relief with appropriate treatment.
• Chronicity: Like enthesitis, enthesopathy can become a chronic issue if not adequately managed. Persistent symptoms can lead to functional limitations and impact quality of life.
• Rehabilitation: Rehabilitation and lifestyle modifications, such as weight management and ergonomic adjustments, can improve outcomes and prevent recurrence.

Early diagnosis and prompt treatment are crucial in managing both enthesitis and enthesopathy effectively. A multidisciplinary approach, involving rheumatologists, physical therapists, and other health care professionals, can optimize patient outcomes. Educating patients about their condition, treatment options, and self-management strategies is essential for long-term success. With appropriate treatment, many patients can achieve good symptom control and maintain a high quality of life.

Preventing enthesitis and enthesopathy can be challenging because they are often associated with underlying conditions such as inflammatory arthritis, overuse injuries, or mechanical stress. However, some strategies can help reduce the risk and manage symptoms:

• Manage underlying conditions: If you have a condition such as psoriatic arthritis, ankylosing spondylitis, or reactive arthritis, following your treatment plan can help manage symptoms and reduce the risk of enthesitis.
• Regular exercise : Engaging in regular, low-impact exercises such as swimming , cycling , or walking can help maintain joint and tendon health. Strengthening exercises can also support the muscles around the joints, reducing stress on the entheses.
• Proper technique: Using proper techniques during physical activities and sports can help prevent overuse injuries. Warm-up exercises before activity and stretching afterward are also beneficial.
• Footwear and orthotics: Wearing appropriate footwear that provides good support can reduce the stress on the lower extremity entheses. Orthotics or insoles may be recommended to correct biomechanical issues.
• Healthy weight: Maintaining a healthy weight reduces the load and stress on weight-bearing joints, which can help prevent enthesitis.
• Anti-inflammatory diet : A diet rich in anti-inflammatory foods, such as fruits, vegetables, omega-3 fatty acids , and whole grains, may help reduce inflammation.
• Avoid overuse: Gradually increase the intensity and duration of physical activities to avoid overuse injuries. Rest and recovery are also essential to prevent overloading the entheses.
• Medical interventions: In some cases, medical interventions such as physical therapy, corticosteroid injections, or biologic medications may be necessary to manage symptoms and prevent recurrence.

Prevention may not always be possible, as some forms of enthesitis are linked to underlying autoimmune or inflammatory conditions. In these cases, managing the root cause is key to preventing recurrent enthesitis episodes.

• Is enthesopathy arthritis?  No. Enthesopathy is a condition that affects the entheses, which are the areas where tendons or ligaments attach to bones. Arthritis, on the other hand, is inflammation of the joints.
• What is the most common site of enthesitis?  The most common site of enthesitis is the heel, particularly at the insertion of the Achilles tendon and the plantar fascia. Other common sites include the backbone, hips, knees, and the underside of the foot.
• Can you exercise with enthesitis?  Yes, you can exercise with enthesitis, but it's important to do it carefully and under the guidance of your doctor or physical therapist. Gentle stretching, strengthening, and aerobic exercises can help reduce pain and stiffness, but avoid high-impact or strenuous workouts during flare-ups. Focus on low-impact activities such as walking, swimming, or cycling, and listen to your body to avoid overexerting yourself. Proper warm-up, stretching, and use of cold therapy after exercise can also help manage symptoms.
• What age does enthesitis occur? Enthesitis can occur at any age but is commonly seen in males between the ages of 6 and 16.

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What Is Enthesopathy and Enthesitis?

By: judith frank, md, rheumatologist.

Peer-Reviewed

A person who has an inflammatory arthritis, particularly a spondyloarthritis such as ankylosing spondylitis or psoriatic arthritis, may experience pain caused by changes to an enthesis (en-THEE-sis). An enthesis is the point where a ligament or tendon attaches to bone. (The plural form is entheses.)

Enthesitis is the first stage in the development of ankylosing spondylitis.

Enthesopathy (en-THEE-sawp-a-thee) is the medical name for any disease or disorder affecting an enthesis. Doctors may use the terms enthesopathy and enthesitis interchangeably—“itis” implies inflammation of the enthesis.

Joints Affected by Enthesopathy

Enthesopathy most commonly affects:

• Feet/heels, especially involving the Achilles tendon (very common) and plantar fascia
• The facet joints that connect the spine’s vertebrae
• The sacroiliac joint between the base of the spine and the pelvis (most common in ankylosing spondylitis)

See Sacroiliac Joint Pain and Inflammation

Enthesopathy can also affect fixed joints. Fixed joints are places where two bones meet but there is little movement. For example, the joints between the breastbone and ribs are fixed joints.

See How Arthritis Causes Joint Pain

How Arthritis Is Related to Enthesopathy

A doctor who diagnoses a patient with enthesopathy will want to identify and treat the underlying cause. In many cases, the underlying cause is systemic (body-wide) inflammation related to arthritis. As inflammation takes place, one or more entheses may become irritated and cause pain.

See Inflammatory Arthritis

Arthritic conditions associated with enthesopathy include but are not limited to:

• Ankylosing spondylitis
• Inflammatory Arthritis
• Psoriatic arthritis
• Septic arthritis

See Types of Arthritis

Trauma and enthesopathy It is possible for enthesopathy to result from a torn tendon or an avulsion fracture (in which a ligament’s or tendon’s enthesis breaks off with a bit of surrounding bone). But in most cases, enthesopathy usually does not result from traumatic injuries.

Treatment for Enthesopathy

There is no specific treatment for enthesopathy, but there are treatments for the underlying diseases that lead to it. These treatments may involve a combination of exercise, activity modification, and medication. Medications can be discussed as a treatment option with your rheumatologist.

See Rheumatologist for Arthritis Treatment

Dr. Judith Frank is a rheumatologist and internal medicine physician. She has been practicing for nearly 30 years, specializing in osteoarthritis, rheumatoid arthritis, gout, and lupus. She completed her Doctor of Medicine degree, residency, and fellowship training from Rush University.

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KEY POINTS • Enthesis represents the site of insertion of tendon, ligament, fascia, or joint capsule into the bone. • Ultrasound is able to visualize the entheseal involvement in the course of many inflammatory and noninflammatory rheumatic diseases. • Power Doppler is important for detecting inflammation of enthesis. The enthesis is the site of insertion of a tendon, ligament, fascia, or joint capsule into the bone ( Fig. 9-1 ). Knowledge regarding the function, anatomy, and physiology of the enthesis has led to improved understanding of entheseal pathology in the course of many inflammatory and noninflammatory rheumatic diseases. F igure 9-1 Schema of Achilles tendon insertion (TA) into the cortical bone includes periosteal fibrocartilage (FP); sesamoid fibrocartilage (FS); calcaneal bursa (BR); connective tissue (TCF), constituted by fibroblasts, not calcified fibrocartilage (FNC), and calcified fibrocartilage (FC); subchondral bone (SCB); bone (B); and vessels (V). (From Breban M, Libbey J [eds]: La Spondylarthrite. Paris, Pathologic Science, 2004.) The two types of enthesis are fibrous and fibrocartilaginous. The latter consists of four anatomic zones: the collagen zone (e.g., ligament, capsule, tendon, aponeurosis, annulus); noncalcified fibrocartilaginous zone; tidemark-calcified fibrocartilaginous zone; and subchondral bone zone. The fibrocartilaginous enthesis is usually observed in the attachment of peripheral muscles. Involvement of the enthesis in any pathologic process—metabolic, inflammatory, traumatic, or degenerative—is referred to as enthesopathy , and the term enthesitis is restricted to inflammatory enthesopathy, which appears to be a cardinal feature of spondylarthritis. Although Niepel and colleagues first used the term for describing inflammatory symptoms at insertional sites as an important feature of ankylosing spondylitis, enthesitis is a common characteristic feature of all spondylarthritis complexes, which include psoriatic arthritis, reactive arthritis, arthritis associated with inflammatory bowel disease, and the undifferentiated forms. In his “Heberden Oration,” Ball suggested that ankylosing spondylitis and rheumatoid arthritis were different primarily in the organs they targeted. He suggested that inflammation at the enthesis is the distinctive pathologic feature of ankylosing spondylitis. In contrast, the characteristic feature of rheumatoid arthritis is a persistent inflammatory synovitis symmetrically involving mainly the peripheral joints. Enthesitis Imaging Findings Understanding the imaging findings of peripheral enthesitis hinges on a thorough knowledge of the joint anatomy. Historically, the radiographic features of enthesitis have played a pivotal role in defining enthesitis lesions of spondylarthritis. They include bone insertion osteopenia, bone cortex irregularity at the insertion, erosion, entheseal soft tissue calcification, and new bone formation ( Fig. 9-2 ). However, entheseal bone changes appear late and are also common in mechanical disorders and in crystal-related pathology. Moreover, aging is associated with an increased prevalence of asymptomatic radiographic enthesopathy . Before the extensive use of magnetic resonance imaging (MRI) and ultrasound for studying inflammatory changes of articular and periarticular structures, scintigraphic studies revealed a diffuse increase in bone and articular uptake in patients with active spondylarthritis. However, the poor spatial resolution of this technique does not permit an anatomic explanation of these findings. F igure 9-2 A, Clinical aspects of enthesitis of the Achilles tendon include swelling and redness of the insertion. B, Radiographic aspects of the Achilles tendon and plantaris fascia enthesitis include erosions (A) and enthesophytes (B). Ultrasound identification of the involvement of entheses in spondylarthritis patients was described for the first time by Lehtinen and colleagues in 1994 and then by Balint and colleagues in 2002. The investigators described the gray-scale abnormalities of lower limb enthesitis of spondylarthritis and the high frequency of asymptomatic findings. Gray-scale ultrasound can depict signs of acute and chronic inflammation of enthesis and show structural damage. Enthesitis seen on gray-scale ultrasound is characterized by the loss of normal fibrillar echogenicity of the tendon insertion with an increased thickness of the insertion or by intralesional focal changes of the tendon insertion, such as calcific deposits, fibrous scars, and periosteal changes (i.e., erosions or new bone formation). Clear involvement of the body of the tendon far from the enthesis and of the adjacent bursae can be observed. Later, discordant data were published about the capability of gray-scale ultrasound to differentiate enthesis involvement in spondylarthritis from involvement in other pathologies, including rheumatoid arthritis. This discordance can be explained by the absence in those studies of a common clear definition of enthesis involvement (most included in such definitions the involvement of tendon and bursa), and by the lack of a clear definition of inflammatory changes by using gray-scale ultrasound only. Inflammation on gray-scale ultrasound mainly is seen as edema, which is characterized by the loss of normal echo structure (associated or not with increased thickness of the tendon insertion) and which is usually difficult to objectively quantify. The use of power Doppler for visualizing abnormal vascularization and hyperemia of soft tissues in inflammatory joint diseases was extensively demonstrated. The first description of the usefulness of power Doppler ultrasound for studying enthesitis was published by D’Agostino and colleagues in 2003. Power Doppler ultrasound was used to detect enthesitis in spondylarthritis patients and in controls (i.e., rheumatoid arthritis patients and mechanical spinal disease patients). Abnormal vascularization at the enthesis insertion was exclusively detected in spondylarthritis patients. This method may permit differentiation of involvement in spondylarthritis from involvement in other mechanical and metabolic disorders. These original results have been confirmed by other studies outlining the ability of power Doppler ultrasound to reveal inflammation of the enthesis in spondylarthritis patients, and the results led to the proposal of several scoring systems. Despite these promising results, power Doppler ultrasound has not been used for the management of spondylarthritis as often as for rheumatoid arthritis. This discrepancy probably can be attributed to the perception that ultrasound is an inseusitive imaging technique and to the greater difficulty of assessing vascular blood flow with Doppler in the entheses than in other tissues such as the synovium, because of the greater abundance of vessels in the inflamed synovium than in the enthesis and because there are more Doppler artifacts at the enthesitic site because of the proximity of a highly reflecting surface, the cortical bone. Another important limitation is the lack of criterion validity. Histologic investigation is considered the gold standard for the demonstration of soft tissue inflammation. In spondylarthritis, because of the difficulties in obtaining tissues for histologic evaluation, there are no studies comparing histologic evidence of inflammation and signs of enthesitis assessed with ultrasound. One small study used ultrasound-guided biopsy of acute Achilles enthesitis in patients with spondylarthritis and sampled regions of gray-scale change and thickening. The procured tissues showed macrophage infiltration, increased vascularity, and edema. Moreover, two histologic studies have demonstrated that aged, normal entheses may have bone microdamage at the enthesis associated with microscope vascular changes, which are likely involved in the repair response. Vascular changes also occur adjacent to enthesophytes in the normal, aged enthesis. This “normal” vascularization cannot be visualized by using power Doppler ultrasound, even when the Doppler signal is enhanced by using medium ultrasound contrast agents. In this context, two competencies are critically needed for sonographers to optimize enthesitis assessment by power Doppler ultrasound: thorough knowledge of the anatomy of each enthesis (particularly the location of normal nutrition vessels), and the ability to differentiate very slow vascular flow (the hallmark of the inflammatory process in the enthesis) from artifacts on power Doppler. Another factor affecting the quality of the ultrasound assessment is the type of Doppler device used. Ultrasound Definition of Enthesitis The Outcome Measures in Rheumatoid Arthritis Clinical Trials (OMERACT) ultrasound group proposed an ultrasound definition for elementary pathologic joint findings, including enthesopathy. These experts decided to define enthesopathy instead of enthesitis to include mechanical and inflammatory pathologies. The preliminary definition of enthesopathy proposed by the OMERACT ultrasound group was an “abnormal hypoechoic (loss of normal fibrillar architecture) and/or thickened tendon or ligament at its bony attachment (may occasionally contain hyperechoic foci consistent with calcification), seen in two perpendicular planes that may exhibit Doppler signal and/or bony changes, including enthesophytes, erosions, or irregularity” ( Fig. 9-3 ). In this definition, acute and chronic inflammatory aspects in gray-scale ultrasound (i.e., loss of normal echo structure, increased thickness, or focal calcific deposits) and Doppler ultrasound are combined with findings of structural damage (i.e., enthesophytes and bony erosions). This combination may be helpful for diagnostic purpose (i.e., presence or absence of enthesis involvement) but probably not for responsiveness or for the differential diagnosis of inflammatory diseases (i.e., spondylarthritis versus rheumatoid arthritis versus mechanical or metabolic entheseal involvement). F igure 9-3 Ultrasound aspects of Achilles tendon enthesitis in a longitudinal view include erosions (A), Doppler signal (B), hypoechogenicity and increased thickness (C), and enthesophytes (D). Normal Ultrasound Aspects of Peripheral Enthesis Under normal conditions, the four zones of fibrocartilaginous enthesis are not visible or are barely visible due to the small thickness of the fibrocartilage and to the quality and resolution of ultrasound equipment ( Fig. 9-4 ). The normal ultrasound aspect of the enthesis is difficult to distinguish from the ultrasound aspect of the body of tendon or ligament, and it appears as a normal continuity of the tendon or ligament into the bone. F igure 9-4 A longitudinal scan shows a normal Achilles tendon insertion. Ultrasound Definitions of Elementary Components of Enthesitis Recently the OMERACT and European League Against Rheumatism (EULAR) ultrasound group tried to standardize the definition of each elementary component contributing to the definition of enthesitis. They first considered enthesitis as involvement of the enthesis, which is different from involvement of the bursa and the body of the tendon. The bursa and tendon can be involved in the inflammatory process of spondylarthritis, but they should be evaluated as different structures and not included in the ultrasound definition of enthesitis. On gray-scale ultrasound, enthesitis is characterized by the following elementary components: • Hypoechogenicity of the insertion of the tendon, ligament, or capsule into the bone, which can be defined as a lack of the homogeneous echotexture pattern with a loss of tightly packed echogenic lines after correcting for anisotropy artifact ( Fig. 9-5 )

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Enthesitis and PsA 

Learn how enthesitis in psoriatic arthritis is detected and treated.

By Timothy Gower

One in three people with psoriatic arthritis (PsA) will develop enthesitis. While this painful problem can affect anyone, enthesitis is far more prevalent, and more likely to become chronic, among people with PsA and other forms of axial spondyloarthritis (such as ankylosing spondylitis). In fact, rheumatologists often look for the presence of enthesitis to help confirm that a patient with joint symptoms has PsA and not another type of arthritis, such as rheumatoid arthritis.

Understanding Enthesitis

While you may not have heard of enthesitis, the structures in the body affected by the condition are involved in every move you make. Bones and muscles are held together with tissues called tendons and ligaments, which allow them to work together and help all types of movement. The site where a tendon or ligament inserts into a bone is called an enthesis. You have more than 100 entheses in your body.

Enthesitis occurs when an enthesis becomes inflamed. Doctors believe that this inflammation is triggered by repeated stress on an enthesis, which causes microscopic damage that builds up over time. The immune system responds to the damage by releasing proteins called cytokines, which cause the enthesis to become inflamed.

Symptoms of enthesitis include pain and stiffness, especially when you move. Constant inflammation may promote abnormal bone growth, producing uncomfortable bone spurs (growths that develop on the edge of a bone). And though no one is quite sure why, enthesitis is closely linked to changes in the finger- and toenails (such as pitting and separation from the nail bed) that affect many PsA patients.

Enthesitis is at the root of some common orthopedic problems brought on by overuse, such as tennis elbow. “However, a person without PsA can apply ice and the enthesitis goes away over time,” says rheumatologist Samantha Shapiro, MD, of UT (University of Texas) Health, Austin. “But in a person with PsA, you have a runaway immune system that continues to inflame the enthesis without normal healing.” That means having PsA predisposes the inflammation to become chronic and require more than ice and time for relief.

Enthesitis often emerges early in PsA, though it can develop at any stage, says rheumatologist Vivian Bykerk, MD, of the Hospital for Special Surgery, in New York City. When the condition arises in people with PsA it can affect the elbows, shoulders, hips and knees, among other areas. But one of the most common targets in PsA is the enthesis where the Achilles tendon attaches to the back of the heel, which can make every footstep a painful experience.

Another common symptom of PsA is just another sign of enthesitis, says Dr. Bykerk. About 40% of people with PsA develop puffy, “sausage-like” fingers and toes, a problem known as dactylitis. “But it’s really a form of enthesitis,” says Dr. Bykerk, since inflammation in the connective tissue of the digits contributes to the swelling.

Diagnosing and Treating Enthesitis

There are no standard lab tests to detect enthesitis. Your doctor may use medical imaging, such as ultrasound, to help determine if you have the condition, but your medical history and symptoms alone provide enough information in most cases, says Dr. Shapiro. For example, if you have pain in back of the heel just above the sole of the foot, swollen joints and finger- and toenail pitting, “then that’s enthesitis,” says Dr. Shapiro. “There’s no need for fancy imaging tests.”

Other conditions, such as fibromyalgia, can produce pain in and around the joints, but a simple test of resistance can help identify enthesitis, says Dr. Bykerk. If a patient describes discomfort in the elbow, for instance, she will ask him to raise that arm. If pushing against his or her palm causes the pain to increase, enthesitis is likely the cause.

“Fibromyalgia tender points won’t have the same level of pain,” says Dr. Bykerk. If your doctor determines you have enthesitis, a change in your treatment plan might be in order.

“Enthesitis really doesn’t respond to oral DMARDs,” says Dr. Shapiro, referring to disease-modifying antirheumatic drugs. These drugs include mainstay medications in the treatment of PsA such as methotrexate and leflunomide. As initial therapy for suspected enthesitis, Dr. Shapiro may try treating a patient with high doses of nonsteroidal anti-inflammatory drugs (NSAIDs) , such as naproxen or indomethacin, for up to a month. But NSAIDs are not an option if you have chronic kidney disease and should be limited or avoided if you have a history of gastrointestinal ulcers or bleeding.

If a patient has enthesitis in just one location, Dr. Bykerk will consider injecting a corticosteroid  to bring down the inflammation. But if symptoms persist or if enthesitis affects several locations in a person with multiple tender joints, then both Drs. Shapiro and Bykerk agree a biologic drug is likely needed.

The first-choice biologic drug for most patients who need one to manage enthesitis or other PsA symptoms will be a TNF inhibitor. There is evidence that TNF inhibitors can quiet enthesitis, says Dr. Shapiro, but not all patients get relief. That’s why researchers are working to validate the effectiveness of IL and JAX inhibitors as well as PDE4 blockers for treating enthesitis.

Authors of a 2018 study published in Current Rheumatology Reports concluded that “the use of different agents including IL-17, IL-23 and JAK inhibitors have contributed significantly to our understanding of diverse immune pathways involved in enthesitis.” The results of different studies have been promising and suggest that these therapeutic agents could prove to be effective treatments.

If you suspect you have enthesitis, tell your doctor right away. He or she can help properly diagnose you and come up with a treatment plan to suit your needs. 

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Introduction

Enthesitis is a central feature of spondyloarthritis (SpA). Although enthesitis has traditionally been considered to be a focal insertional disorder, advanced imaging and pathologic findings suggest that enthesitis is a diffuse process with effects on adjacent bone and soft tissue. As a result of repeated biomechanical stress, it appears that microdamage at the enthesis triggers an inflammatory response in the synovium, leading to synovitis. Along with mechanical stress, exogenous bacteria may play a role in activating the immune response, especially in genetically predisposed individuals whose major histocompatibility locus encodes the class I molecule HLA–B27. Recent studies in animal models suggest that autoimmunity against versican and fibrocartilage proteins, and bone morphogenetic protein (BMP) signaling play roles in enthesitis development. Finally, interleukin-23 (IL-23) has been implicated in enthesitis with inflammatory effects mediated through IL-17 and tumor necrosis factor (TNF), and new bone formation driven by IL-22.

Although prior therapeutic choices were limited to nonsteroidal antiinflammatory drugs (NSAIDs) and activity modification, in recent years TNF inhibitors have proven to be useful. Further research on the effects of IL-22 and IL-23 blockade is needed to understand the effects on the treated patient. While enthesitis is underdiagnosed by physical examination alone, the use of ultrasound has proven to be highly sensitive for the detection of enthesitis, with utility in monitoring response to therapy, and will be an invaluable tool for assessing the efficacy of newer treatments. This review summarizes the substantial progress that has been made in addressing the pathophysiology, molecular mechanisms, genetic associations, clinical features, diagnostic modalities, and treatment of enthesitis.

Definitions and evolution of the enthesis concept

Historic definition.

Although the adjective “enthetic” derives from the ancient Greek word “enthetikos,” meaning “introduced into the body from without,” in the nineteenth century the adjective was increasingly used to refer to diseases that were “implanted into the body from external sources” ( 1 ). It was not until the twentieth century that the term “enthesis” was used as it is today, referring to focal insertional abnormalities at sites of bony attachments to tendons, ligaments, fascia, muscles, or joint capsules ( 2 , 3 ). The first suggestion that the enthesis is centrally affected in SpA was made by Ball in 1971 and was substantiated after a review of pathologic tissues from both patients with rheumatoid arthritis (RA) and patients with ankylosing spondylitis (AS), where he noted the presence of a unique inflammatory enthesopathy that could help to distinguish SpA from RA ( 2 ).

Broadening the definition of enthesis with the concept of the “enthesis organ”

Magnetic resonance imaging (MRI) and ultrasound findings have suggested that enthesopathy encompasses pathologic changes extending to the adjacent bone and soft tissues ( 4 ). Likewise, it has been argued that this entity should be considered an “enthesis organ” encompassing not only the enthesis itself, but also the fibrocartilage, bursa, fat pad, adjacent trabecular bone networks, and deeper fascia ( 5 ) ( Figure 1 ). Representing areas where hard and soft tissues meet, entheses are sites of concentrated stress with effects not only on the bony attachment interface and the enthesis itself, but also on these neighboring tissues ( 4 – 7 ).

Illustration of the Achilles enthesis organ.

Entheses and mechanical stress

The concept of an enthesis organ was extended to that of a synovioentheseal complex ( 8 , 9 ), which refers to the relationship between the proinflammatory synovium and the avascular enthesis. In contrast to other skeletal locations, the enthesis is a site of repetitive biomechanical forces. High biomechanical stress at the enthesis triggers an inflammatory cascade with cytokine production by infiltrating monocytes and lymphocytes in the adjacent synovial tissue, resulting in an articular inflammatory response, and clinically leading to synovitis adjacent to attachment sites ( 8 , 9 ). Support for this theory of a dynamic response to biomechanical stress at the enthesis originates from animal models. In one experiment, botulinum toxin A injection delayed fibrocartilage development, suggesting that enthesis development is sensitive to mechanical environmental factors ( 10 ). In a mouse model that overexpresses TNF, enthesitis was reduced when the hind legs of the mice were made non–weight-bearing through tail suspension ( 11 ). Those authors proposed that triggering of mechanoreceptors via the MAPK pathway stimulates the production of inflammatory mediators.

As a result of biomechanical stress, adjacent bone reacts with formation of surface spurs or enthesophytes, observed both radiographically and on histologic examination ( 12 ). In early disease, there is destruction of superficial fibrocartilage, with vascular invasion and inflammatory cell infiltration, predominantly with macrophages ( 13 ). This leads to another important microanatomical feature, which is the presence of blood vessels at sites where synovium, subchondral bone, and bone marrow are close to each other. In early experiments using labeled phosphorus, Ball identified capillary-like vessels that pass through the enthesis to the marrow ( 2 ). Later studies described the presence of vascular channels penetrating cortical bone in the knees of mice adjacent to the cruciate ligaments with associated subclinical changes, including subchondral bone damage and microcyst formation. In the rat adjuvant-induced arthritis model, vascular channels provided a site for inflammatory tissue entry and osteoclast activation ( 14 ).

Whether enthesitis is a primary central lesion or a secondary process remains a matter of debate. Studies that have implicated enthesitis as the primary process include studies of TNF-transgenic mice, in which the earliest lesion appears to be in the enthesis ( 11 ). However, this may be model specific, and a number of reports have challenged the idea of enthesitis as the primary inflammatory lesion ( 15 , 16 ). In one study examining different stages of spontaneous tail spondylitis and peripheral arthritis in HLA–B27/h β 2 m–transgenic mice, histologic samples displayed destructive synovitis with neutrophils and multinucleated giant cells rather than by enthesitis or osteitis ( 16 ). Among human studies examining biopsy specimens and MRIs of sacroiliac joints, synovitis and subchondral bone marrow changes were more prominent features while enthesitis was not ( 17 , 18 ). In a subsequent study, in patients with early untreated knee or ankle arthritis, analyses revealed a higher synovitis score by MRI in SpA than in RA, whereas there were no differences in the prevalence of enthesitis as assessed by perientheseal focal tissue, entheseal enhancement, and bone marrow edema ( 15 ). However, in light of substantial data in animal models highlighting 3 stages of tendon response to injury that have been defined by distinct pathologic changes, determining the initiating event in the enthesis may be confounded by the timing of the analysis ( 19 – 21 ).

Contributing cellular and molecular mechanisms

Genetic susceptibility.

It has long been known that AS susceptibility is largely genetically determined. The strongest genetic association is with the major histocompatibility complex (MHC)–encoded class I molecule, HLA–B27, and it is postulated that HLA–B27 contributes to ~40% of the overall risk for SpA ( 22 ). Protein misfolding of nascent HLA–B27 in the endoplasmic reticulum has been hypothesized to trigger an unfolded protein response with aberrant recognition by natural killer cell receptors ( 23 ). The HLA–B27–induced unfolded protein response in macrophages has been demonstrated in HLA–B27–transgenic rats and is associated with an increase in IL-23 production by these cells ( 24 ). Although HLA–B27 remains the dominant risk factor for susceptibility to the AS phenotype, other important influences of the MHC have been observed ( 25 ). More recently, Haroon et al ( 26 ) found a positive association of B*27:05:02 with enthesitis, dactylitis, and symmetric sacroiliitis in a cohort of psoriatic arthritis (PsA) patients, whereas B*44 haplotypes were associated with a decreased frequency of enthesitis, dactylitis, and joint fusion. Finally, investigators have recently focused on genes outside of the MHC region, such as ERAP1 and ERAP2, which code for aminopeptidases that are involved in MHC class I presentation ( 25 , 27 ). Although additional HLA class I and class II alleles have also been implicated, the scale and scope of gene identification to date have not yet matched the putative total genetic risk for SpA.

Microbial factors

Microbial infection with virulent organisms remote from affected joints, as well as gastrointestinal dysbiosis without a directly invading pathogen, are known features of certain phenotypes of SpA, and it has long been appreciated that microbial factors can lead to immune activation ( 28 ). Clinically, reactive arthritis (ReA) is known to follow infections with Chlamydia , Campylobacter , Shigella , or Yersinia . AS patients consistently have been found to have subclinical gut inflammation and increased gastrointestinal permeability ( 29 , 30 ). In animal models, HLA–B27–transgenic rats raised in germ-free environments do not develop intestinal inflammatory or peripheral joint disease, yet the disease recurs if rats are reconstituted with Bacteroides , supporting the role of gut flora in the development of joint inflammation ( 31 ). In a more recent study, colonoscopic biopsies of the terminal ileum of AS patients showed a discrete microbial signature as revealed by sequencing and quantitative polymerase chain reaction analysis of the 16S ribosomal RNA (16S rRNA) gene, exhibiting higher levels of 5 families of bacteria as compared to healthy controls ( 32 ). In that study there was no significant difference in the 16S rRNA copy number between patients with AS and controls, indicating that the observed differences were not due to bacterial overgrowth. It has been postulated that the combination of bacterial adjuvants and mechanical factors act synergistically to activate the immune response, particularly in genetically predisposed individuals ( 5 ).

Fibrocartilage and versican autoimmunity

A number of studies have indicated that autoimmunity against fibrocartilage proteins, including aggrecan, may underlie enthesitis and spondylitis ( 33 ). A model of SpA induced by immunizing BALB/c mice with the G1 globular domain of versican, leading to spondylitis and enthesitis, suggests that versican autoimmunity may also play a role in enthesitis ( 34 ). The inflammatory lesions are characterized by mononuclear cell infiltration at the entheseal insertions to the vertebrae, as is seen with AS, and are associated with angiogenesis which then progresses to cause destructive discitis ( 35 ).

Role of bone morphogens

In the DBA/1 mouse model, where mice develop spontaneously occurring arthritis that culminates in bone formation and joint ankylosis, male mice in crowded conditions developed arthritis in the hind paws that was entheseal, but not synovially based, with new bone formation driven by BMP-7 signaling ( 36 ). In that experiment, the incidence of arthritis was increased in mice that were caged together in crowded conditions, yet decreased when the mice were placed in larger cages ( 37 ). Thus, in addition to a genetic predisposition for enthesitis, this observation points to the role of environmental factors in the development of arthritis. Finally, immunohistochemical studies in SpA show increased synovial expression of BMP-2 and BMP-6, which is up-regulated by proinflammatory cytokines such as IL-1 and TNF, suggesting that synovial molecules contribute to chronic arthritis and joint ankylosis ( 36 , 38 ).

Role of proinflammatory cytokines

The role of IL-23 has been addressed as a major driver of cascades that lead to inflammation and bone remodeling in SpA. Alterations in AS susceptibility are related to the existence of single-nucleotide polymorphisms in the IL-23 receptor as demonstrated in genome-wide association studies, and serum levels of the IL-12/23 p40 subunit have been shown to be significantly higher in patients with PsA compared with controls ( 39 , 40 ). IL-23 is produced in the gut, suggesting that the intestinal mucosa is a key site of IL-23 production in SpA. Additionally, Chlamydia trachomatis also leads to induction of IL-23 via CHOP10. Taken together, these findings indicate that IL-23 is a pivotal cytokine and potentially central to the pathogenesis of SpA ( 41 ). Increased IL-17 expression by innate immune cells such as mast cells and neutrophils in SpA has been shown to target the facet joints and synovial tissue ( 42 , 43 ). In a subsequent set of investigations, Sherlock et al found that IL-23 could induce SpA by acting on an isolated population of CD3+CD4−CD8− entheseal resident lymphocytes, leading to increased expression of TNF and IL-6 in the enthesis. When IL-23 was overexpressed, mice developed enthesitis with inflammation, which spread into the adjacent synovium ( 41 ). Enthesitis was associated with new bone erosion. IL-23 promoted inflammation through IL-17 and TNF, whereas new bone formation was associated with overproduction of IL-22 ( 41 , 44 ) ( Figure 2 ).

Interleukin-23 (IL-23) is activated via a variety of pathways including the HLA–B27 unfolded protein response. IL-23 then activates resident T cells within the enthesis, which then promotes inflammation and bone remodeling, with inflammation mediated by IL-17 and osteoproliferation mediated by IL-22. The net result is bone ankylosis in the spine. ROR γ t = retinoic acid receptor–related orphan nuclear receptor γ t; TNF = tumor necrosis factor. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/journal/doi/10.1002/art.39458/abstract

Additional support for the role of IL-23 comes from the SKG mouse model, in which curdlan ( β -1,3-glucan) injections induce enthesitis and dactylitis. Arthritis and spondylitis were IL-23 dependent and were transferable to SCID mouse recipients with CD4+ T cells ( 45 ). In this model, disease severity was dependent on the external microbial environment and the host immunogenetic background. More recent work illustrates the differential impact of microbiota on specific pathologic features of SpA; ileitis development, ileal IL-23 expression, and lymph node IL-17A production were microbiota dependent, but arthritis was not ( 46 ). In curdlan-treated SKG mice, enthesitis was specifically dependent on IL-17A and IL-22 ( 47 ). The role of up-regulation of the IL-23/Th17 pathway in promoting joint inflammation and bone turnover is further supported by recent murine studies, with inhibition of the PsA phenotype after neutralization of IL-17A ( 48 , 49 ).

Clinical enthesitis in SpA

SpA is by definition a heterogeneous group of clinical entities long recognized as having unique phenotypes that include AS, ReA, PsA, enteropathic arthritis, and what has traditionally been referred to as undifferentiated arthritis. However, with advances in imaging and careful long-term followup observations, it appears that these diseases share common features, including subclinical spinal and peripheral joint inflammation, along with associations with microbes and gene identifications. In attempting to develop a model for an underlying unifying anatomical basis for SpA, an “enthesitis-based model” has been proposed as the basis for the osteitis, periostitis, and new bone formation that are seen in SpA ( 5 ). The association between enthesitis and adjacent osteitis has been further supported by imaging and cadaver studies, primarily in patients with PsA ( 50 – 52 ).

Regional sites

Patients with SpA have a remarkable propensity for inflammation at certain enthesis sites that are ubiquitous and numerous. Clinically, peripheral enthesitis is observed not only in all forms of SpA, but particularly frequently in juvenile-onset SpA. A number of patients with juvenile SpA are classified as having enthesitis-related arthritis (ERA), a heterogeneous subtype that includes some patients who predominantly have enthesitis, enthesitis and arthritis, or juvenile AS. Compared to other subtypes of juvenile idiopathic arthritis, ERA is associated with worse function, worse quality of life, and increased pain ( 53 , 54 ).

Enthesitis can be seen in 33–58% of patients with ReA and may be the only clinical manifestation in some whose disease has been triggered by an enteric infection ( 55 ). In SpA, the entheses of the lower extremities are more frequently involved than those of the upper limbs, and the heel is the most frequent site ( 55 ). In addition to the Achilles and plantar fascia insertions, identified sites of enthesitis include muscle attachments to the greater and lesser trochanters, the insertion of the quadriceps tendon at the upper patellar pole, the insertions of the patellar ligament at the lower patellar pole and the tibial tubercle, acromial and clavicular insertions of the deltoid muscle, and the insertions of the flexor and extensor tendons at the phalanges ( 55 – 57 ). It is unknown why there is a predilection for the entheses at the lower parts of the lower limbs, although it has been hypothesized that this may be due to the length, anatomy, and higher mechanical load at these sites.

Given the presumed role of repetitive biomechanical forces discussed above, it is not surprising that in patients with longstanding AS, those with occupational activities that required more bending, twisting, and stretching had more functional limitations and radiographic damage than those whose jobs required little or no dynamic flexibility ( 58 ). A recently published computer-based method that fully quantified syndesmophyte heights and volumes on computed tomography scans has revealed that syndesmophytes grow at different rates over time in AS patients, suggesting that mechanical factors local to the disc space may influence syndesmophyte formation ( 59 ). Clearly, there are sites that are not associated with SpA despite being sites of significant biomechanical stress, and perhaps it is the compressive and shear force nature of the stress as well as the putative role of antigen expression adjacent to the enthesis that may underlie this apparent discrepancy ( 5 ). Additionally, it cannot be discounted that the increased detection of enthesitis at the lower limbs is explained by the accessibility of these sites to ultrasound.

Diagnostic criteria and outcome measures

Enthesitis is often underdiagnosed in the clinic; clinical assessment and quantification of peripheral enthesitis in daily practice lacks sensitivity and specificity ( 56 , 60 , 61 ). Although both the Amor criteria ( 62 ) and the European Spondylarthropathy Study Group criteria ( 63 ) for SpA include peripheral enthesitis, there are limitations to these criteria with regard to the exact quantification of enthesitis. Two clinical methods have been designed and often implemented for evaluating enthesopathy in AS: Mander’s Entheseal Index and the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) ( 64 , 65 ). Both rely on pain elicited by local pressure of entheseal points. The intraarticular and deep location of entheseal insertions, however, makes quantification of enthesitis by physical examination alone difficult, and not surprisingly, these scoring systems have only moderate sensitivity and specificity for predicting positive sonogram results, depending on the entheseal site ( 66 ).

Imaging of the enthesis

Because of the clinical limitations described above and the poor sensitivity of markers of inflammation, it is necessary to rely on typical abnormalities seen on various imaging techniques to diagnose SpA. Plain radiographs are limited by their inability to show inflammation or soft tissue changes, although late chronic bony changes such as enthesophyte formation or occasional erosions can be seen at the attachment of the Achilles tendon or plantar aponeurosis. More sensitive methods such as ultrasound and MRI, which are useful in their ability to detect both inflammatory and chronic changes in enthesitis at both early and late stages, can be used.

MRI has changed the way we approach both the diagnosis and classification of SpA; it is particularly useful in detecting spinal disease in early AS when conventional radiographs are still normal ( 67 ). The use of fat-suppressed, fat-saturated, and water-sensitive MRI sequences has demonstrated that the extracapsular inflammation of joints quite often represents enthesitis with variable degrees of soft tissue and bone marrow edema ( 68 , 69 ) ( Figures 3 – 5 ). The typical appearance of enthesitis on MRI includes soft tissue inflammatory changes outside the joint capsule and perientheseal bone marrow edema ( 70 ). Recent studies have examined the utility of whole-body MRI, which has shown promise in the detection of subclinical axial and peripheral enthesitis ( 71 ). Of course, MRI has limitations; structures that make up entheses have a low signal on conventional MRI, with low water accumulation in the areas where fibroblasts are tightly cross-linked. MRI is further limited by its cost and availability, and therefore ultrasound remains the preferred modality for the detection of enthesitis both in the clinical setting as well as in research.

Achilles tendon insertion into the calcaneus. An abnormal signal is seen at the posterior calcaneus at the site of the Achilles entheseal insertion (encircled area) on magnetic resonance imaging using STIR sequences. Reproduced from ref. 68 .

Fat-suppressed T1-weighted sequence magnetic resonance image (MRI) of the right midfoot of a 58-year-old woman with HLA–B27–positive peripheral spondyloarthropathy. The MRI demonstrates extensive enthesitis, synovitis, and tenosynovitis of the peroneus longus, peroneus brevis, tibialis posterior, flexor digitorum longus, and extensor digitorum tendons. This is characterized by excess fluid and enhancement in and around the tendon sheaths. Arrow indicates extensive edema and enhancement at the plantar aspect of the midfoot, involving insertions of intrinsic musculature and capsular ligaments consistent with enthesitis. Image courtesy of Dr. Joseph Robinson (Cedars-Sinai Medical Center).

Ultrasound has indeed proven to be a highly useful and sensitive tool in the evaluation of enthesitis and improves the ability of the clinical examination to detect enthesopathy. In one study of 92 patients with PsA, ultrasound was useful in detecting subclinical entheseal involvement, independent of clinical examination and symptoms ( 72 ). In another study of 600 lower limb entheses, at least 1 ultrasound sign of enthesopathy was detected in 60% of clinically asymptomatic cases of enthesitis, thus demonstrating a higher sensitivity than physical examination ( 73 ).

Ultrasound may be most useful in the early diagnosis of SpA, and likewise, entheseal abnormalities can be detected prior to overt clinical disease. Nevertheless, in an older cross-sectional single-center study of 51 SpA patients and 24 controls, neither MRI nor power Doppler ultrasound (PDUS) discriminated between SpA and controls ( 74 ). In a prospective single-center cohort study of 118 patients with symptoms suggestive of SpA conducted by D’Agostino and colleagues ( 57 ), vascularization at cortical bone detected by PDUS of at least one enthesis provided good predictive value for diagnosing SpA with a sensitivity of 76.5% and a specificity of 81.3%. Indeed, PDUS is a sensitive and reliable technique used to detect increased blood flow in the enthesis revealing neovascularity and subclinical active inflammation ( 56 , 75 ) ( Figure 6 ).

A, Ultrasound image of a patient with psoriatic arthritis with enthesitis (long-axis view of the lateral epicondyle [high-frequency, 18-MHz probe]). Precise delineation of blood flow seen at the cortical interface on B-flow imaging is shown. Calcification is seen adjacent to the epicondyle. B and C, 3T magnetic resonance image of the same patient, in the same orientation as the ultrasound in A, showing proton density (B) and fat presaturation (C). Boxed areas show the region of the lateral epicondyle. Images courtesy of Dr. Ralph Thiele (University of Rochester, Rochester, NY). Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/journal/doi/10.1002/art.39458/abstract

Recent studies have indicated that ultrasound may accurately predict which patients will go on to develop SpA ( 51 , 57 , 75 ). In one investigation, ultrasound examination of Achilles erosions correlated with objective activity-based measurements of SpA outcomes, and was sensitive to change ( 76 ). In the study by D’Agostino and colleagues described above, vascularized enthesis as detected by PDUS combined with Amor’s criteria proved to be the only independent contributors to a diagnosis of SpA ( 57 ).

Finally, ultrasound may be used to monitor response to therapeutic interventions. A few studies have illustrated improvement in enthesitis shown on ultrasound after the use of TNF antagonists ( 77 , 78 ). In one investigation of 327 patients with active SpA who were treated with anti-TNF therapy for 6 months, cumulative entheseal morphologic abnormalities, intraenthesis and perienthesis, and bursitis were all significantly decreased on PDUS after 6 months of treatment ( 77 ). In another study, D’Agostino et al monitored regression of enthesitis using PDUS after treatment with infliximab ( 78 ), providing confirmatory evidence for the utility of ultrasound in a clinical research setting.

Treatment of enthesitis

Historically, treatment of clinical enthesitis had been limited to NSAIDs. Continuous use of NSAIDs not only controls symptoms of disease, but may also slow progression of bony changes in AS ( 79 , 80 ). Therefore, Assessment of SpondyloArthritis international Society/European League Against Rheumatism guidelines place optimal NSAID therapy as a cornerstone of the management plan for AS ( 81 ).

Treatment with TNF inhibitors is indicated in patients that do not respond to NSAID therapy. TNF inhibition with adalimumab, etanercept, infliximab, and golimumab has been shown to be efficacious in the treatment of enthesitis ( 82 – 87 ). Olivieri et al ( 88 ) have reported that adalimumab and etanercept are effective treatments of MRI-documented refractory heel enthesitis, with progressive improvement of bone edema in a 6-month period ( 88 ).

Agents that block IL-23 have the potential to inhibit both inflammation and altered bone remodeling, although further analysis of the effect of IL-22 and IL-23 blockade on bone pathologies in animal models and patients with PsA are needed to address this important therapeutic issue ( 89 ). Entheseal inflammation in a passive-transfer model of collagen antibody-induced arthritis was reduced by an antibody to the p19 subunit of IL-23, which was also associated with the down-regulation of several inflammatory mediators, such as IL-6 and IL-1 β , and genes such as Rankl , Ctsk , and matrix metalloproteinases known to be involved in bone erosion ( 41 ). Both ustekinumab, a monoclonal antibody directed against the common p40 subunit of IL-12 and IL-23, and secukinumab, a human anti–IL-17A monoclonal antibody, have already demonstrated promise in PsA, with significant improvements in enthesitis ( 90 , 91 ).

Apremilast, an oral inhibitor of phosphodiesterase 4, which increases cAMP and thus modulates multiple proinflammatory mediators, has demonstrated efficacy in PsA, with significant improvements in the severity of both enthesitis and dactylitis evidenced by reductions in MASES over a 52-week period ( 92 ). Finally, bisphosphonates may also have a role in peripheral enthesitis felt to be refractory to NSAID therapy. In a 6-month randomized controlled comparison of intravenous pamidronate treatment of NSAID-refractory AS, patients treated with pamidronate showed symptomatic improvement with significant reductions in Bath Ankylosing Spondylitis Functional Index and Bath Ankylosing Spondylitis Disease Activity Index measurements together with regression of periarticular osteitis documented by MRI with gadolinium ( 93 ).

Treatment of patients with SpA enthesitis with currently available agents has not had universal success. In placebo-controlled trials of methotrexate and leflunomide in PsA, enthesitis measures were not assessed ( 94 , 95 ). In a randomized controlled trial, sulfasalazine was not effective for enthesitis ( 96 ). Other agents that have not demonstrated clinical efficacy in AS include tocilizumab, and lymphocyte-targeted therapies such as abatacept ( 97 , 98 ). Rituximab only showed modest therapeutic efficacy in SpA ( 99 , 100 ).

Conclusions

In summary, investigations and clinical observations uniformly point out with increasing clarity that the enthesis is much more than a simple attachment site. A number of studies have shown that it functions as a unit comprising adjacent tissues, including bone and fibro-cartilage linked to synovium, and serves as a way of dissipating stress over a wide area. Inflammation at the enthesis manifests in the adjacent synovium presumably via immunity to common antigens or via release of proinflammatory cytokines at the enthesis. Although work by Benjamin and McGonagle ( 9 ) suggests that the enthesis is the primary SpA lesion, the precise role of the enthesis in early stages of disease, especially regarding issues of cause or effect, remains an area of continued debate and discovery. Improved imaging modalities may in the future be able to detect enthesitis at different stages of disease. However, this will require a clinically diverse and large sample size to help address this question. Inflammation at the enthesis is likely modulated by multiple factors. A more complete role for genetic predisposition will require additional advances in gene sequencing and discovery. Repeated biomechanical stress with the resultant inflammatory response regulated by IL-17, IL-22, and IL-23 now provide clues as to why certain areas of the body are affected, and perhaps why others are not. The spine itself (the clinical hallmark of the disease) remains inaccessible to traditional enthesitis-focused research methodologies thus far. However, newer imaging techniques are on the horizon. Further examination into the role of the inflammatory mediators, including IL-17, IL-22, and IL-23 as well as potentially others, in driving enthesitis and bone formation will be important to direct our attention toward future therapeutic targeted pathways in patients with SpA.

Radiographic findings of enthesitis in a 21-year-old man with ankylosing spondylitis. A, Reference plain radiograph. B, Magnetic resonance image with T1 sequence showing a small erosion at the right greater trochanter. C, Axial T2 fat-saturated sequence of the right hip showing edema of the right gluteus minimus tendon at its insertion, consistent with enthesitis. Arrows indicate the region of the right greater trochanter. Images courtesy of Dr. Joseph Robinson (Cedars-Sinai Medical Center).

Acknowledgments

Supported in part by the NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases grant P01-AR-052915 and National Center for Advancing Translational Sciences grant UL1-TR-000124).

The authors wish to thank Joseph Robinson, MD (Cedars-Sinai Medical Center Department of Radiology) for assistance with MRI acquisition and interpretation.

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Enthesopathy of Hip: Causes, Symptoms, Treatment

What is enthesopathy of hip.

To understand about Enthesopathy of Hip, it is important to understand what does enthesopathy mean? The areas where the tendons and ligaments attach to the bone are called enthesis. When these areas get inflamed and painful then that condition is called Enthesopathy. 1

Thus, when the area where tendons and ligaments attach to the hip bone becomes inflamed then it leads to development of what is called as Enthesopathy of Hip. This is basically an arthritic disorder and affects the normal functioning of the hip.

An individual with Enthesopathy of Hip will find it difficult to move the hip in any direction and will also find it difficult to ambulate normally. The affected individual will also find it very tough to carry out activities of daily living due to pain and decreased range of motion of the hip as a result of Enthesopathy of Hip.

The majority of the changes due to Enthesopathy of Hip are seen at the femoral head of the hip and the joint acetabulum while the anterior capsule is the portion of the hip that is least affected by Enthesopathy of Hip. Of late, PRP injections have shown great promise in treating acute cases of Enthesopathy of Hip.

What are the Causes Of Enthesopathy of Hip?

Some of the common causes of Enthesopathy of Hip are:

• Inflammatory disorders affecting the hip like rheumatoid arthritis can cause enthesopathy of hip 2
• Psoriatic arthritis is yet another condition that can affect the hip and cause Enthesopathy of Hip
• Reactive arthritis is also a medical condition that may cause Enthesopathy of Hip
• Osteoarthritis is a common cause of Enthesopathy of Hip
• Other medical conditions like Crohn’s disease or Reiter’s syndrome can also cause Enthesopathy of Hip

Apart from this any physical injury or trauma to the hip like a slip and fall or a motor vehicle accident can also cause Enthesopathy of Hip. Additionally, recreational drug abuse, some sort of infection, or a surgical procedure to the hip like a hip debridement for arthritis or a replacement may also cause Enthesopathy of Hip.

What are the Symptoms of Enthesopathy of Hip?

Some of the symptoms of Enthesopathy of Hip are:

• Severe pain with movement of the hip
• Decreased range of motion of the hip 2
• Problems with ambulation due to pain and discomfort at the hip
• Hip soreness.

How is Enthesopathy of Hip Treated?

The treatment for Enthesopathy of Hip is generally conservative and includes utilization of NSAIDs for calming down the pain and inflammation. The NSAIDs may either be given topically or orally depending on the severity of the pain. 3 The most preferred medications for treatment of Enthesopathy of Hip are acetaminophen and naproxen.

If NSAIDs are not effective in treating the patient’s symptoms then the next step towards treatment is steroid injections to bring down the inflammation due to Enthesopathy of Hip.

If both of these agents fail to provide any relief then medications like Humira or Enbrel which are anti-TNF agents are used to treat Enthesopathy of Hip. In addition to the medications, the patient will have to undergo aggressive physical therapy to regain lost range of motion and strength of the hips as a result of Enthesopathy of Hip.

The physical therapy may use modalities like ultrasound, electric stimulation, and massage as a mode of strengthening the hip and bring back the range of motion lost due to Enthesopathy of Hip.

References:  

• https://www.ncbi.nlm.nih.gov/pubmed/3924467
• https://www.medicalnewstoday.com/articles/318987.php
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5195265/
• Hip Sprain: Causes, Symptoms, Treatment, Exercises
• Post Traumatic Osteoarthritis of the Hip Joint: Causes, Signs, Treatment, Exercises
• Q&A: Hip Joint Pain Treatment Approach and Options–Everything You Need To Know

Hip Joint Rheumatoid Arthritis: Causes, Signs, Symptoms, Treatment

Hip joint septic arthritis: causes, symptoms, treatment, pt, surgery.

• Hip Joint Psoriatic Arthritis: Causes, Symptoms, Treatment, PT, Surgery

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Citation, DOI, disclosures and article data

At the time the article was created Jeremy Jones had no recorded disclosures.

At the time the article was last revised Daniel J Bell had no financial relationships to ineligible companies to disclose.

• Footprint (tendon attachment)
• Footprints (tendon attachment)

An enthesis (plural: entheses), also known, more informally, as a footprint , generally refers to the anatomic junction where connective tissue (e.g. ligament , tendon , joint capsule , bursa or a combination thereof) attaches to bone.

Entheses are commonly classified into two types 1 :

fibrocartilage

In a fibrous enthesis, the collagen fibers comprising ligament or tendon attach directly to periosteum or bone cortex 1,2 . They are usually associated with short tendons, e.g. gluteus maximus insertion onto the femur 1 . This usually occurs along a relatively wide area of a bone shaft 1 .

Fibrocartilage

A fibrocartilage enthesis represent a more complex attachment between tendon and bone. They generally occur at locations where tendon inserts onto a portion of bone lacking periosteum, e.g. an epiphysis.

They are classically divided into four zones:

collagen zone - derived from tendon or other soft tissue structure

non-calcified fibrocartilaginous zone - variable thickness where chondrocytes predominate

calcified fibrocartilaginous zone - an abrupt transition ("tidemark" or "blue line")

subchondral bone zone

The zonal organization is thought to result in decreased stress on the interface 1 .

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Related pathology

enthesopathy : a pathological condition affecting the enthesis

enthesitis : an inflammatory condition causing enthesopathy

enthesophyte : bony projection at an enthesis in response to enthesopathy

• 1. Anthony S. Tadros, Brady K. Huang, Mini N. Pathria. Muscle-Tendon-Enthesis Unit. (2018) Seminars in Musculoskeletal Radiology. 22 (03): 263. doi:10.1055/s-0038-1641570 - Pubmed
• 2. D'Agostino MA, Terslev L. Imaging Evaluation of the Entheses: Ultrasonography, MRI, and Scoring of Evaluation. (2016) Rheumatic diseases clinics of North America. 42 (4): 679-693. doi:10.1016/j.rdc.2016.07.012 - Pubmed
• 3. William Palmer, Laura Bancroft, Fiona Bonar, Jung-Ah Choi, Anne Cotten, James F. Griffith, Philip Robinson, Christian W.A. Pfirrmann. Glossary of terms for musculoskeletal radiology. (2020) Skeletal Radiology. doi:10.1007/s00256-020-03465-1 - Pubmed

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• Cortical bone
• Prepatellar quadriceps continuation
• Enthesopathy
• Myotendinous unit
• Enthesophyte
• Enthesopathy vs enthesitis (diagram)

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