Acute enthesitis is inflammation at the site where a tendon, ligament, or joint capsule attaches to bone (the enthesis). This inflammation develops rapidly—often within days—and causes pain, swelling, and impaired function. Unlike chronic enthesitis, which evolves over weeks or months, acute enthesitis is characterized by a sudden onset, frequently triggered by injury, infection, or an underlying inflammatory disease. Understanding acute enthesitis is crucial for early diagnosis and management, as timely intervention can relieve pain, restore mobility, and prevent progression to chronic damage.
Acute enthesitis is inflammation that occurs at an enthesis—the specific site where a tendon, ligament, or joint capsule attaches to bone. Unlike tendonitis, which affects the body of a tendon, enthesitis specifically involves the insertion point and often extends into adjacent bone and soft tissue, making it a diffuse inflammatory process rather than a purely focal one PMCScienceDirect. It is most commonly seen in spondyloarthropathies (such as ankylosing spondylitis and psoriatic arthritis), but can also arise from overuse, trauma, or infection Wikipedia.
Pathophysiology
At the microscopic level, the enthesis is a complex biomechanical zone composed of tendon or ligament fibers, a fibrocartilaginous transition zone, mineralized fibrocartilage, and bone. In acute enthesitis, mechanical stress or inflammatory mediators (e.g., cytokines like TNF-α and interleukin-17) disrupt this zone, leading to increased blood flow, immune cell infiltration (neutrophils and macrophages), and release of enzymes that degrade collagen and proteoglycans. The resulting tissue edema and cellular activation produce the characteristic pain and swelling at the bone attachment site.
Types of Acute Enthesitis
Inflammatory Enthesitis in Spondyloarthritis
Seen in conditions like ankylosing spondylitis and psoriatic arthritis, this type arises from systemic immune-mediated inflammation targeting the enthesis. Patients often have genetic predispositions (e.g., HLA-B27 positivity) and concurrent axial or peripheral joint involvement.Mechanical (Overuse) Enthesitis
Repetitive stress—common in athletes, manual laborers, or individuals with poor ergonomics—can microdamage the enthesis. When repair mechanisms are overwhelmed, acute inflammation ensues, particularly at weight-bearing sites like the Achilles tendon.Calcific Enthesitis
Deposition of calcium hydroxyapatite crystals within the enthesis triggers an acute inflammatory response. Although more frequent in chronic settings, an acute flare (“calcific tendinitis”) can cause severe pain and localized swelling.Septic Enthesitis
Bacterial or fungal pathogens (e.g., Staphylococcus aureus) can seed the enthesis via the bloodstream or from adjacent infections. Rapid-onset pain, warmth, and systemic signs (fever, elevated white count) distinguish septic enthesitis and require urgent antimicrobial therapy.Traumatic Enthesitis
Acute trauma—such as a sudden pull or direct blow—can partially tear the enthesis and provoke a robust inflammatory response. Falls, sprains, or impact injuries commonly precipitate this type of enthesitis.Crystalline Enthesitis (Gout and Pseudogout)
Monosodium urate (gout) or calcium pyrophosphate dihydrate (pseudogout) crystals can accumulate at the enthesis, triggering acute flares characterized by intense pain, erythema, and swelling.
Causes of Acute Enthesitis
Spondyloarthropathies:
Genetic and immune factors converge in ankylosing spondylitis and psoriatic arthritis to drive sudden enthesis inflammation. Enthesitis often appears early, before joint space narrowing occurs.Repetitive Mechanical Stress:
Prolonged running, jumping, or heavy lifting can overload the enthesis, leading to microtears and acute inflammatory reactions.Direct Trauma:
A fall or impact can bruise or partially tear the enthesis, initiating an inflammatory cascade for tissue repair.Calcific Deposits:
Hydroxyapatite crystals accumulate and intermittently shed into surrounding tissues, provoking acute inflammation.Infectious Seeding:
Bacteria or fungi enter via the bloodstream or contiguous spread, localize at the enthesis, and trigger acute purulent inflammation.Crystal Arthropathies:
Sudden precipitation of urate (gout) or calcium pyrophosphate crystals triggers intense, acute inflammatory responses in entheses.Metabolic Disorders:
Hyperparathyroidism and other metabolic imbalances can alter bone turnover and predispose tendon insertions to inflammation.Obesity:
Excess weight increases mechanical load on entheses in the lower limbs, raising the risk of overuse enthesitis flares.Poor Biomechanics:
Foot pronation, limb length discrepancies, or improper footwear can unevenly distribute forces, stressing specific entheses acutely.Diabetes Mellitus:
Microvascular impairment and glycation of collagen make entheses more susceptible to injury and slow healing, facilitating acute inflammatory episodes.Steroid Injections:
Paradoxical local inflammation can follow intralesional corticosteroid, causing transient acute enthesitis as a side effect.Tendon Overstretching:
Sudden excessive stretching, as in rapid athletic maneuvers, may partially tear fibers where tendon meets bone.Autoimmune Conditions:
Beyond spondyloarthritis, disorders like rheumatoid arthritis or systemic lupus erythematosus can on occasion present with acute enthesitis.Viral Infections:
Certain viruses (e.g., parvovirus B19) can transiently localize in musculoskeletal tissues, causing acute enthesis pain.Medication-Induced:
Drugs such as fluoroquinolones are linked with tendinopathy and can precipitate acute enthesitis through direct collagen toxicity.
Symptoms of Acute Enthesitis
Localized Pain:
Sharp, focal pain at the tendon or ligament insertion, often described as “burning” or “throbbing.” This pain intensifies with movement or pressure.Tenderness on Palpation:
Light touch or pressing over the enthesis elicits discomfort, distinguishing enthesitis from deeper joint pain.Swelling:
Accumulation of inflammatory fluid around the enthesis leads to visible or palpable swelling at the bone attachment site.Warmth and Redness:
Increased blood flow produces local heat and erythema, especially in septic or crystalline enthesitis.Stiffness:
Patients often report difficulty moving the affected limb, particularly after periods of rest (e.g., first steps in the morning).Pain with Resisted Movement:
Actively contracting the muscle inserting at the enthesis (e.g., calf contraction for Achilles) reproduces or worsens pain.Functional Limitation:
Activities such as walking, climbing stairs, or lifting objects become challenging, impairing daily living.Morning Stiffness:
Enthesis inflammation tends to “set” overnight; stiffness lasting more than 30 minutes is common in inflammatory spondyloarthritis.Night Pain:
Pain that awakens patients from sleep, often signaling active inflammation rather than mechanical overuse.Crepitus or Cracking:
Subtle grating sensations may be felt if calcific deposits or irregular enthesis surfaces rub during movement.
Diagnostic Tests for Acute Enthesitis
Physical Examination Tests
Palpation of Enthesis
The clinician uses firm pressure over the tendon insertion to identify the exact point of maximal tenderness, confirming the enthesis as the pain source.Range of Motion Assessment
Passive and active joint movements are evaluated; decreased flexibility or pain at end-range suggests adjacent enthesitis.Functional Gait Analysis
Observing walking patterns can reveal limp or altered biomechanics due to pain at lower-limb entheses (e.g., Achilles, plantar fascia).Hoffman’s Sign for Achilles
With the patient prone, squeezing the calf reproduces pain at the Achilles enthesis if inflammation is present.Pain with Resisted Contraction
The examiner resists a muscle contraction (e.g., plantarflexion) to isolate enthesis pain from muscle belly pain.
Manual Provocative Tests
Metatarsal Squeeze Test
Compressing the forefoot from sides provokes pain at the plantar fascia insertion, indicating acute enthesitis in pes planus.Patellar Tendon Squeeze
Squeezing the patellar tendon just below the kneecap stresses its tibial insertion, reproducing pain in patellar enthesitis.Elbow Epicondyle Compression
Applying pressure to the lateral or medial epicondyle tests for tennis or golfer’s elbow enthesitis, respectively.Resisted Dorsiflexion Test
The patient dorsiflexes the foot against resistance; pain at the tibialis anterior insertion indicates enthesitis there.
Laboratory and Pathological Tests
Erythrocyte Sedimentation Rate (ESR)
An elevated ESR signals systemic inflammation and supports an inflammatory etiology of enthesitis.C-Reactive Protein (CRP)
High CRP levels correlate with active inflammation and help monitor response to therapy.Rheumatoid Factor (RF) and Anti-CCP Antibodies
Used to exclude rheumatoid arthritis when enthesitis occurs outside spondyloarthropathies.Serum Uric Acid
Elevated levels suggest gout-related crystalline enthesitis, guiding specific management.Enthesis Biopsy and Histopathology
Rarely performed but definitive: biopsy shows inflammatory cell infiltrate, collagen breakdown, and, if present, infectious organisms or crystals.
Electrodiagnostic Tests
Electromyography (EMG)
Helps rule out primary muscle or nerve disorders; normal EMG with localized pain points to enthesitis rather than neuropathy.Nerve Conduction Studies
Excludes compressive neuropathies that can mimic enthesitis by causing distal limb pain.Ultrasound Elastography
Measures tissue stiffness at the enthesis; increased stiffness supports acute inflammation with edema.
Imaging Tests
Plain Radiography (X-ray)
May show periosteal reaction, bone spur formation, or calcifications at the enthesis in acute flares overlying chronic changes.Ultrasound Imaging
High-resolution ultrasound detects tendon thickening, hypoechoic areas (fluid), and Doppler signal indicating active inflammation.Magnetic Resonance Imaging (MRI)
Gold standard for early enthesitis: MRI visualizes bone marrow edema, soft-tissue swelling, and contrast enhancement at the enthesis.
Non-Pharmacological Treatments
Below are evidence-based, non-drug strategies grouped into physiotherapy/electrotherapy modalities, exercise therapies, mind-body approaches, and educational/self-management programs.
A. Physiotherapy & Electrotherapy Therapies
Therapeutic Ultrasound
Description: Uses high-frequency sound waves delivered via a transducer and coupling gel to the skin.
Purpose: To reduce pain, improve range of motion, and promote tissue healing in the acute phase.
Mechanism: Thermal effects increase tissue temperature and blood flow; non-thermal effects enhance cell permeability and stimulate collagen synthesis Wikipedia.Transcutaneous Electrical Nerve Stimulation (TENS)
Description: Delivers low-voltage electrical currents through skin electrodes.
Purpose: Provides fast, localized pain relief without drugs.
Mechanism: Activates large-diameter Aβ fibers to “gate” pain signals in the spinal cord and promotes endogenous opioid release Wikipedia.Extracorporeal Shockwave Therapy (ESWT)
Description: High-energy acoustic waves focused on the enthesis.
Purpose: Alleviates chronic insertional pain and stimulates tissue repair.
Mechanism: Mechanical stress induces microtrauma, triggering neovascularization and growth factor release Complete Physio.Cryotherapy (Cold Therapy)
Description: Application of ice packs or cold compresses to the inflamed enthesis.
Purpose: Rapidly reduces pain and swelling in acute flares.
Mechanism: Vasoconstriction limits inflammatory mediator flow; cold also slows nerve conduction to reduce pain perception PMC.Thermotherapy (Heat Therapy)
Description: Use of hot packs or heating pads over subacute/chronic enthesitis.
Purpose: Relieves stiffness and promotes muscle relaxation.
Mechanism: Increases local blood flow, enhances tissue extensibility, and soothes muscle spasms Wikipedia.Manual Therapy (Massage & Mobilization)
Description: Hands-on techniques by a physiotherapist to mobilize soft tissues and joints.
Purpose: Restores normal biomechanics, reduces pain, and prevents adhesions.
Mechanism: Mechanical loading stimulates mechanoreceptors, inhibits nociceptors, and improves lymphatic drainage ResearchGate.Iontophoresis
Description: Uses a mild electrical current to drive anti-inflammatory agents (e.g., acetic acid) into tissue.
Purpose: Delivers medication directly to the enthesis without needles.
Mechanism: Electromigration enhances transdermal drug penetration, reducing local inflammation and pain ClinMed Journals.Low-Level Laser Therapy (LLLT)
Description: Applies low-intensity laser light to inflamed areas.
Purpose: Promotes cellular repair and reduces pain.
Mechanism: Photobiomodulation increases mitochondrial ATP production, modulates cytokines, and enhances microcirculation Physiopedia.Interferential Current Therapy (IFC)
Description: Medium-frequency currents intersect to produce low-frequency stimulation in deeper tissues.
Purpose: Pain relief, reduction of edema, and muscle re-education.
Mechanism: Produces analgesia by gate control and stimulates endorphin release; the beat frequency penetrates deeper than TENS Wikipedia.Pulsed Electromagnetic Field Therapy (PEMF)
Description: Uses time-varying electromagnetic fields to target the enthesis region.
Purpose: Reduces inflammation and accelerates bone and soft tissue healing.
Mechanism: Modulates ion channels and cellular signaling pathways involved in inflammation and tissue regeneration Wikipedia.
B. Exercise Therapies
Range of Motion (ROM) Exercises
Description: Gentle, controlled movements through the joint’s full capacity.
Purpose: Maintains joint mobility and prevents stiffness.
Mechanism: Promotes synovial fluid distribution and prevents contractures eular.org.Strengthening Exercises
Description: Targeted isometric or low-resistance muscle contractions around the enthesis.
Purpose: Provides tendon/ligament support and reduces load on the insertion site.
Mechanism: Improves muscular stability and attenuates excessive mechanical stress eular.org.Stretching Exercises
Description: Static or dynamic stretches of muscles and tendons crossing the enthesis.
Purpose: Decreases tension at the insertion point and enhances flexibility.
Mechanism: Lengthens soft tissue, reduces microtears, and improves compliance eular.org.Aquatic Therapy
Description: Low-impact exercises performed in warm water.
Purpose: Minimizes weight-bearing load while allowing strengthening and ROM.
Mechanism: Buoyancy reduces joint compression; hydrostatic pressure supports edema reduction eular.org.Proprioceptive Training
Description: Balance and coordination drills (e.g., single-leg stance).
Purpose: Enhances neuromuscular control to protect the enthesis.
Mechanism: Improves joint position sense, reducing abnormal loading patterns eular.org.
C. Mind-Body Therapies
Yoga
Description: Combines gentle postures with breath control.
Purpose: Improves flexibility, reduces stress-related muscle tension, and modulates pain perception.
Mechanism: Activates parasympathetic responses, decreases cortisol, and enhances mechanotransduction in connective tissues.Tai Chi
Description: Slow, flowing movements with mindfulness.
Purpose: Enhances joint mobility and proprioception while reducing stress.
Mechanism: Low-impact loading stimulates cartilage health and downregulates inflammatory pathways.Mindfulness Meditation
Description: Focused attention and awareness exercises.
Purpose: Reduces pain catastrophizing and improves coping with chronic symptoms.
Mechanism: Alters central pain processing via modulation of the anterior cingulate and insular cortices.
D. Educational & Self-Management
Patient Education Programs
Description: Structured sessions on disease understanding and lifestyle modifications.
Purpose: Empowers patients to recognize flare triggers and adhere to treatment plans.
Mechanism: Knowledge reduces anxiety, improves self-efficacy, and promotes active participation in care PMC.Self-Management Strategies
Description: Includes activity pacing, joint protection techniques, and use of orthoses/braces.
Purpose: Minimizes overload on entheses and prevents symptom exacerbation.
Mechanism: Balances between rest and activity to allow repair without deconditioning.
Key Drugs for Acute Enthesitis
First-line pharmacotherapy often targets inflammation and immune modulation. Below are ten commonly used agents:
Ibuprofen (NSAID)
Class: Non-steroidal anti-inflammatory drug
Dosage: 200–400 mg PO every 4–6 hours as needed; OTC max 1,200 mg/day; prescription up to 3,200 mg/day Medscape Reference
Timing: With meals to reduce GI upset
Side Effects: GI bleeding, renal impairment, hypertension
Naproxen (NSAID)
Class: Non-selective NSAID
Dosage: 250–500 mg PO twice daily; maximum 1,500 mg/day MPR
Timing: Morning and evening doses with food
Side Effects: GI ulceration, cardiovascular risk
Indomethacin (NSAID)
Class: Non-selective NSAID
Dosage: 25–50 mg PO 2–3 times daily
Timing: Food-related dosing to minimize GI effects
Side Effects: Headache, GI upset, fluid retention
Celecoxib (COX-2 Inhibitor)
Class: Selective COX-2 inhibitor
Dosage: 100–200 mg PO once or twice daily
Timing: With or without food
Side Effects: Lower GI risk but higher CV risk in susceptible patients
Diclofenac (NSAID)
Class: Non-selective NSAID
Dosage: 50 mg PO 2–3 times daily; topical 1–4% gel applied 3–4 times daily
Timing: With meals
Side Effects: GI irritation, hepatic enzyme elevation
Methylprednisolone (Corticosteroid Injection)
Class: Glucocorticoid
Dosage: 20–40 mg intra-enthesis injection once
Timing: Single outpatient procedure
Side Effects: Local pain flare, infection risk, systemic absorption effects
Sulfasalazine (DMARD)
Class: Disease-modifying antirheumatic drug
Dosage: Start 500 mg PO daily, titrate to 2 g/day in divided doses
Timing: With food
Side Effects: GI upset, rash, oligospermia
Methotrexate (DMARD)
Class: Antimetabolite
Dosage: 7.5–15 mg PO or SC once weekly
Timing: Weekly dosing with folic acid supplementation
Side Effects: Hepatotoxicity, cytopenias, mucositis
Etanercept (TNF Inhibitor)
Class: Biologic DMARD
Dosage: 50 mg SC once weekly
Timing: Self-administered injection
Side Effects: Injection site reactions, infection risk
Secukinumab (IL-17A Inhibitor)
Class: Biologic DMARD
Dosage: 150 mg SC at weeks 0, 1, 2, 3, 4, then every 4 weeks
Timing: Loading dose then maintenance
Side Effects: Candidiasis, neutropenia, infection risk
Dietary Molecular Supplements
These agents may offer adjunctive anti-inflammatory or tissue-support benefits.
Omega-3 Fatty Acids
Dosage: 1–3 g/day of EPA/DHA
Function: Anti-inflammatory eicosanoid shift
Mechanism: Competes with arachidonic acid for COX/LOX enzymes
Curcumin
Dosage: 500 mg twice daily PubMed
Function: Potent anti-inflammatory antioxidant
Mechanism: Inhibits NF-κB and COX-2 pathways
Boswellia Serrata Extract
Dosage: 300 mg TID of 65% boswellic acids
Function: Reduces leukotriene-mediated inflammation
Mechanism: 5-LOX inhibition
Ginger (Zingiber officinale)
Dosage: 250 mg TID of standardized extract
Function: Analgesic and anti-inflammatory
Mechanism: Inhibits prostaglandin and leukotriene synthesis
Methylsulfonylmethane (MSM)
Dosage: 1,500 mg TID
Function: Reduces joint pain and oxidative stress
Mechanism: Sulfur donor for collagen synthesis and antioxidant support
Vitamin D₃
Dosage: 1,000–2,000 IU daily
Function: Modulates immune response and supports bone health
Mechanism: Regulates T-cell differentiation and cytokine production
Type II Collagen
Dosage: 10 mg daily
Function: Supports cartilage matrix integrity
Mechanism: Oral tolerance induction and chondroprotection
Glucosamine Sulfate
Dosage: 1,500 mg daily
Function: Stimulates glycosaminoglycan synthesis
Mechanism: Provides substrate for cartilage repair
Chondroitin Sulfate
Dosage: 1,200 mg daily
Function: Maintains extracellular matrix hydration
Mechanism: Inhibits degradative enzymes in cartilage
Bromelain
Dosage: 500 mg TID on an empty stomach
Function: Anti-edematous and analgesic
Mechanism: Proteolytic enzyme reducing bradykinin-mediated swelling
Advanced Therapies
These targeted agents may be considered for refractory cases or regeneration purposes.
Alendronate (Bisphosphonate)
Dosage: 70 mg PO once weekly
Function: Reduces bone turnover at enthesis
Mechanism: Inhibits osteoclast-mediated bone resorption
Zoledronic Acid (Bisphosphonate)
Dosage: 5 mg IV once yearly
Function: Long-term suppression of enthesis bone remodeling
Mechanism: Binds hydroxyapatite and inhibits osteoclasts
Platelet-Rich Plasma (PRP)
Dosage: Autologous injection 3–5 mL, 1–3 sessions
Function: Delivers growth factors to promote repair
Mechanism: Concentrates PDGF, TGF-β, VEGF to stimulate tissue regeneration
Dextrose Prolotherapy (Regenerative)
Dosage: 10–20% dextrose injection monthly for 3 sessions
Function: Provokes controlled inflammation for repair
Mechanism: Hyperosmolar solution triggers fibroblast proliferation
Hyaluronic Acid (Viscosupplementation)
Dosage: 2–4 mL injection weekly for 3–5 weeks
Function: Enhances lubrication and shock absorption
Mechanism: Restores viscoelasticity of synovial fluid at entheseal bursa
Autologous Mesenchymal Stem Cell Injection
Dosage: 1–5 × 10⁶ cells per injection, 1–2 sessions
Function: Differentiates into tenocytes and modulates inflammation
Mechanism: Paracrine signaling to promote tissue repair and immune regulation
Surgical Procedures
Reserved for severe, refractory enthesitis with structural damage.
Enthesectomy
Procedure: Surgical removal of inflamed enthesis tissue
Benefits: Eliminates chronic nidus of inflammation and pain
Debridement
Procedure: Arthroscopic removal of fibrous scar and calcifications
Benefits: Restores tendon gliding and relieves impingement
Osteotomy
Procedure: Bone realignment to unload the enthesis (e.g., calcaneal osteotomy)
Benefits: Redirects stress away from damaged insertion
Tendon Transfer
Procedure: Replaces damaged tendon insertion with a healthier tendon
Benefits: Restores function when primary repair is not feasible
Plantar Fascia Release (for plantar enthesitis)
Procedure: Partial or complete release of plantar fascia origin
Benefits: Reduces tension and alleviates heel pain
Prevention Strategies
Maintain healthy body weight to reduce enthesis loading
Warm up adequately before physical activity
Use appropriate footwear and orthoses for shock absorption
Incorporate strength training to balance muscle forces
Stretch regularly to preserve tendon flexibility
Avoid sudden increases in activity intensity or duration
Gradually return to sport after injury
Use ergonomic tools and postures at work
Quit smoking to enhance tissue healing
Ensure adequate vitamin D and calcium for bone health
When to See a Doctor
Persistent enthesis pain > 4 weeks despite self-care
Severe swelling, redness, or warmth suggesting infection
Systemic symptoms (fever, chills, malaise)
Progressive functional limitations or gait changes
Neurological signs (numbness, weakness) in adjacent regions
“What to Do” & “What to Avoid”
Do:
Ice the area 15 min after activity
Perform prescribed ROM and strengthening exercises
Use NSAIDs as directed for acute flares
Seek physiotherapy guidance early
Incorporate cross-training to reduce repetitive stress
Avoid:
High-impact sports during acute phase
Running or jumping on hard surfaces
Sudden loading without gradual progression
Ignoring early signs of enthesis pain
Prolonged complete immobilization without therapeutic exercise
Frequently Asked Questions (FAQs)
What exactly is an enthesis?
An enthesis is the site where connective tissue such as a tendon, ligament, or joint capsule attaches to bone.How does enthesitis differ from tendonitis?
Enthesitis affects the insertion point at bone, whereas tendonitis involves inflammation of the tendon body.Which conditions commonly cause enthesitis?
Spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis), overuse injuries, and infections can all lead to enthesitis.Can I continue exercising with enthesitis?
Low-impact, guided exercises (e.g., aquatic therapy) are encouraged, but high-impact activities should be avoided during acute inflammation.Are NSAIDs always necessary?
NSAIDs are first-line for pain and inflammation, but non-pharmacological strategies can reduce reliance on drugs.When are injections indicated?
Corticosteroid injections are considered when pain persists despite NSAIDs and physiotherapy.Is surgery often required?
Surgery is a last resort, reserved for structural damage or failed conservative management.Do supplements really help?
Some molecular supplements (e.g., omega-3, curcumin) have evidence supporting modest anti-inflammatory effects.How long does recovery take?
Mild cases may improve in weeks; more severe enthesitis can take months of combined therapy.Can enthesitis become chronic?
Yes—if not addressed early, repeated inflammation can lead to bone spur formation and lasting pain.Is enthesitis contagious?
No—enthesitis is not an infectious disease unless directly caused by infection at the site.Will physical therapy make it worse?
Properly guided, graded physiotherapy should improve symptoms; aggressive therapy without supervision may exacerbate pain.Can diet influence enthesitis?
A balanced diet rich in anti-inflammatory nutrients (omega-3s, antioxidants) may support overall management.How do I know if it’s an enthesitis flare?
Flare signs include localized redness, warmth, and worsening pain at the insertion site after activity or rest.Where can I find more information?
Reliable sources include rheumatology societies (EULAR, ACR), clinical guidelines, and your healthcare provider.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: July 11, 2025.
