Fibrocartilaginous Enthesitis

Fibrocartilaginous enthesitis is inflammation at the site where a tendon, ligament, or joint capsule attaches to bone—specifically at an enthesis that normally contains fibrocartilage. In healthy adults, these fibrocartilaginous entheses act as shock absorbers, gradually transferring stress from soft tissue to bone. When overloaded by mechanical stress, autoimmune activity, metabolic disturbance, or microtrauma, the fibrocartilage becomes inflamed. This inflammation can erode the attachment, weaken the tendon or ligament, and eventually lead to calcification or ossification if left untreated. Fibrocartilaginous enthesitis is distinct from fibrous enthesitis—in which the attachment zone contains mainly dense connective tissue—because it involves a specialized fibrocartilage layer that changes both the risk factors and healing response.

Entheses are the sites where tendons, ligaments, or joint capsules attach to bone, and can be classified as fibrous (direct periosteal insertions) or fibrocartilaginous (with zones of uncalcified and calcified fibrocartilage bridging tendon to bone) NCBIWikipedia. Fibrocartilaginous enthesitis refers to inflammation centered at these fibrocartilaginous enthesis organs, characterized by microdamage from repetitive mechanical stress, a cytokine-driven immune response (IL-17, TNF, IL-23), and consequent synovio-entheseal inflammation that may extend into adjacent bone and soft tissues PMCRheumatology Advisor. Clinically, this manifests as focal pain, tenderness, and sometimes swelling at sites like the Achilles tendon, plantar fascia, or lateral epicondyle, and is a hallmark of spondyloarthropathies (e.g., psoriatic arthritis, ankylosing spondylitis) Rheumatology AdvisorWikipedia.

Under the microscope, affected entheses show increased cellularity, infiltration by immune cells (particularly macrophages and lymphocytes), proliferation of fibroblasts and chondrocyte-like cells, and early calcific deposits. Over weeks to months, the body may attempt repair by laying down new fibrocartilage, but chronic or repetitive insults can lead to fibrocartilage degeneration, bony spurs, and persistent pain. Clinically, patients report localized pain, tenderness, and sometimes swelling over the insertion site, often worsened by movement that stretches or compresses the affected tissue. Early recognition and treatment are crucial to prevent chronic changes and functional impairment.

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Types of Fibrocartilaginous Enthesitis

1. Acute Fibrocartilaginous Enthesitis
   In the acute phase—usually lasting days to a few weeks—immune cells flood the fibrocartilage in response to injury or systemic inflammation. Patients feel sharp, local pain aggravated by motion. Microscopically, there is edema and early fibroblast activation but minimal scar or bone formation.

2. Subacute (Proliferative) Enthesitis
   Between two and six weeks after onset, the enthesis shows active fibroblast and chondrocyte proliferation. The body attempts to repair damage by generating new fibrocartilage matrix. Symptoms may plateau or even improve temporarily, though patients often report stiffness and mild discomfort rather than sharp pain.

3. Chronic (Degenerative) Enthesitis
   After six weeks, repeated stress or insufficient resolution leads to degenerative changes: breakdown of normal fibrocartilage, replacement by fibrous scar tissue, and sometimes micro-tears. Pain becomes more constant, and function may be limited. Imaging may show thinning of the fibrocartilage layer and early calcific deposits.

4. Calcific/Ossifying Enthesopathy
   In longstanding cases, calcium crystals deposit in the damaged enthesis, eventually ossifying into bone spurs or enthesophytes. Patients often describe deep, aching pain and may have palpable bony lumps. Surgical removal of spurs is sometimes necessary if conservative treatments fail.

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Causes of Fibrocartilaginous Enthesitis

1. Repetitive Mechanical Overload
   High-impact activities—running, jumping, manual labor—repeatedly stress fibrocartilaginous entheses. Over time, micro-injuries accumulate faster than the body can repair them, triggering inflammation.

2. Direct Trauma
   A single heavy blow or sudden stretch (e.g., landing awkwardly) can tear the fibrocartilage, provoking an inflammatory response and pain at the tendon or ligament insertion.

3. Age-Related Degeneration
   With aging, fibrocartilage becomes less elastic and more brittle. Normal activities that were once harmless can start micro-tearing the enthesis, especially after age 40.

4. Obesity and Increased Body Mass
   Excess weight amplifies forces on lower extremity entheses (e.g., Achilles, patellar tendon), increasing the risk of overload and inflammation.

5. Ankylosing Spondylitis
   This inflammatory arthritis often targets fibrocartilaginous entheses along the spine and pelvis. Immune-mediated attacks on entheses lead to chronic pain and eventual spinal fusion if untreated.

6. Psoriatic Arthritis
   In psoriatic disease, enthesitis (including fibrocartilaginous sites) is a hallmark feature. Skin and joint inflammation can coincide at multiple insertion sites, causing pain and swelling.

7. Reactive Arthritis
   Following certain infections, immune complexes may deposit at fibrocartilaginous entheses, leading to pain days to weeks after the initial illness.

8. Enteropathic Arthritis (IBD-Associated)
   Patients with Crohn’s or ulcerative colitis frequently experience enthesitis, with fibrocartilage‐rich sites like the pubic symphysis often affected.

9. Gout
   Uric acid crystals can accumulate at entheses, including fibrocartilaginous insertions, triggering intense inflammation and often causing misdiagnosis as tendonitis.

10. Diabetes Mellitus
    Chronic high blood sugar and associated microvascular changes impair tendon blood supply and healing, making fibrocartilaginous entheses more prone to degeneration and inflammation.

11. Hyperparathyroidism
    Elevated parathyroid hormone disrupts calcium metabolism, leading to calcification at fibrocartilage and subsequent enthesitis.

12. Diffuse Idiopathic Skeletal Hyperostosis (DISH)
    Enthesophyte formation and calcification affect multiple fibrocartilaginous entheses, particularly along the spine, causing pain and stiffness.

13. Fluorosis
    Excess fluoride intake can lead to abnormal fibrocartilage mineralization at entheses, provoking chronic inflammation.

14. Overuse in Sports
    Athletes who repeatedly perform sport-specific movements (e.g., volleyball spikes stressing the deltoid insertion) frequently develop enthesitis at fibrocartilaginous sites.

15. Steroid Injections
    While steroid injections reduce inflammation acutely, repeated injections near an enthesis can weaken tendons and fibrocartilage over time, precipitating degeneration and enthesitis.

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Symptoms of Fibrocartilaginous Enthesitis

1. Localized Pain at the Insertion Site
   Patients describe a sharp or aching pain exactly where the tendon or ligament attaches to bone. Moving or stretching the tissue often reproduces the pain immediately.

2. Tenderness on Palpation
   Pressing directly over the enthesis elicits discomfort or sharp pain, distinguishing it from deeper joint pain that may require different tests.

3. Swelling and Mild Warmth
   In acute phases, the affected area may swell slightly and feel warmer than the surrounding skin, indicating active inflammation.

4. Stiffness, Especially after Rest
   Patients often report stiffness when first moving after periods of rest (e.g., morning stiffness)—a sign of synovial-like involvement around the enthesis.

5. Reduced Range of Motion
   Pain and swelling may limit how far a joint can flex or extend, impacting activities like climbing stairs or raising the arm overhead.

6. Functional Weakness
   Inflammation can weaken the tendon or ligament attachment, reducing strength in associated movements (e.g., plantar flexion in Achilles enthesitis).

7. Crepitus or Grinding Sensation
   Damaged fibrocartilage may create a subtle grinding or crackling feeling when the tendon glides over its bony insertion.

8. Night Pain
   Many patients notice worsening discomfort at night, potentially due to decreased distraction, lower cortisol levels, or prolonged pressure on the enthesis.

9. Muscle Guarding
   Surrounding muscles may spasm reflexively to protect the inflamed enthesis, causing secondary pain and tightness.

10. Visible Bony Lumps in Chronic Cases
    Longstanding enthesitis can lead to palpable bone spurs (“enthesophytes”) that patients may notice as hard nodules near the insertion.

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Diagnostic Tests for Fibrocartilaginous Enthesitis

Physical Examination Tests

1. Direct Palpation
   The clinician applies steady pressure over the enthesis. Sharp pain exactly at the insertion, but not over the muscle belly or joint line, supports enthesitis.

2. Range-of-Motion Assessment
   The affected joint is passively moved. Pain at specific angles—such as dorsiflexion aggravating Achilles enthesitis—helps localize the pathology.

3. Functional Loading Test
   The patient actively uses the muscle and tendon (e.g., single-leg heel raise). Pain or weakness during the test indicates enthesis involvement.

4. Gait Analysis
   Observing how a patient walks can reveal compensatory limping, reduced push-off strength, or altered stride length suggestive of lower-extremity enthesitis.

Manual (Provocative) Tests

5. Resisted Movement Test
   The examiner resists the patient’s contraction of the involved muscle (e.g., resisted plantar flexion for Achilles). Pain during contraction pinpoints enthesis injury.

6. Compression (Squeeze) Test
   For the plantar fascia insertion, squeezing the heel’s sides provokes pain if fibrocartilaginous enthesitis is present.

7. Cross-Body Adduction Test
   In shoulder enthesitis (e.g., deltoid insertion), crossing the arm across the body compresses the enthesis and reproduces pain.

8. Palpation with Ultrasound Probe
   Combining manual pressure with ultrasonographic visualization helps correlate tenderness with structural changes under live imaging.

Laboratory and Pathological Tests

9. Erythrocyte Sedimentation Rate (ESR)
   Elevated ESR reflects systemic inflammation that often accompanies inflammatory enthesitis in conditions like ankylosing spondylitis.

10. C-Reactive Protein (CRP)
    CRP rises rapidly in acute inflammation, helping distinguish inflammatory from purely mechanical causes of enthesis pain.

11. Rheumatoid Factor and Anti-CCP
    Although more relevant for synovial arthritis, these autoantibodies can help rule out rheumatoid involvement when enthesitis is suspected.

12. HLA-B27 Genetic Test
    A positive HLA-B27 marker strongly suggests spondyloarthropathy-related enthesitis, especially when axial sites are involved.

13. Serum Uric Acid
    Elevated levels point toward gouty enthesitis, where urate crystals deposit at fibrocartilaginous insertions.

14. Tissue Biopsy (Rarely Used)
    In atypical or refractory cases, a biopsy of the enthesis can identify crystal deposits, infection, or other pathological processes.

Electrodiagnostic Tests

15. Electromyography (EMG)
    EMG helps exclude nerve entrapment or radiculopathy by assessing muscle electrical activity; a normal EMG in the presence of pain points back to enthesitis.

16. Nerve Conduction Studies (NCS)
    NCS confirm that symptoms are not due to peripheral neuropathy—if conduction is intact, enthesis inflammation is more likely the culprit.

Imaging Tests

17. Plain Radiography (X-Ray)
    X-rays can show bony spurs (enthesophytes) at chronic enthesitis sites, though early changes are often missed.

18. Ultrasound
    High-resolution ultrasound visualizes thickening, tears, or calcifications in the fibrocartilage, and power Doppler can detect active blood flow in inflamed entheses.

19. Magnetic Resonance Imaging (MRI)
    MRI is the gold standard for early detection: it reveals bone marrow edema at the enthesis, fibrocartilage tears, and soft-tissue inflammation before X-ray changes appear.

20. Computed Tomography (CT)
    CT precisely delineates calcific deposits and enthesophytes, aiding surgical planning in chronic, ossifying cases.

Non-Pharmacological Treatments

A multimodal, non-pharmacological approach is essential for managing enthesitis, aiming to reduce inflammation, promote healing, and restore function JRheum.

Physiotherapy & Electrotherapy

1. Extracorporeal Shock Wave Therapy (ESWT)

   • Description: High-energy acoustic pulses delivered to the enthesis.

   • Purpose: Alleviate pain and stimulate tissue repair.

   • Mechanism: Induces microtrauma that promotes neovascularization, growth factor release, and collagen synthesis ResearchGate.

2. Low-Level Laser Therapy (LLLT)

   • Description: Non-thermal laser light applied over the affected area.

   • Purpose: Reduce pain and inflammation.

   • Mechanism: Photobiomodulation enhances mitochondrial activity, leading to decreased cytokine release and increased cell proliferation PubMed.

3. Therapeutic Ultrasound

   • Description: High-frequency sound waves transmitted via a skin probe.

   • Purpose: Improve tissue extensibility and reduce pain.

   • Mechanism: Thermal effects increase blood flow; non-thermal cavitation and microstreaming promote cell repair Wikipedia.

4. Transcutaneous Electrical Nerve Stimulation (TENS)

   • Description: Surface electrodes deliver pulsed electrical currents.

   • Purpose: Provide analgesia.

   • Mechanism: Gate control of pain and release of endogenous opioids Wikipedia.

5. Interferential Current Therapy (ICT)

   • Description: Two medium-frequency currents intersect to produce low-frequency stimulation.

   • Purpose: Deep pain relief and muscle stimulation.

   • Mechanism: Enhanced tissue penetration reduces nociceptive signaling and promotes blood flow PMC.

6. Cryotherapy

   • Description: Application of cold packs or ice.

   • Purpose: Decrease acute inflammation and pain.

   • Mechanism: Vasoconstriction limits inflammatory mediator delivery, reduces nerve conduction velocity.

7. Heat Therapy

   • Description: Warm packs or paraffin baths.

   • Purpose: Alleviate stiffness and pain.

   • Mechanism: Vasodilation increases tissue extensibility and metabolite clearance.

8. Manual Therapy (Joint Mobilization)

   • Description: Skilled passive movements by a therapist.

   • Purpose: Improve joint mechanics and reduce pain.

   • Mechanism: Mechanotransduction promotes synovial fluid distribution and modulates nociception.

9. Massage Therapy

   • Description: Soft-tissue manipulation (e.g., effleurage, petrissage).

   • Purpose: Reduce muscle tension and enhance circulation.

   • Mechanism: Mechanical pressure breaks adhesions and stimulates lymphatic drainage.

10. Dry Needling

    • Description: Fine needles inserted into trigger points near the enthesis.

    • Purpose: Decrease pain and improve tissue function.

    • Mechanism: Local twitch response and neurophysiological modulation of pain pathways.

Exercise Therapies

11. Stretching Exercises

    • Targets tight muscle–tendon units to improve flexibility.

12. Strengthening Exercises

    • Focuses on the muscles crossing the enthesis (e.g., calf raises for Achilles enthesitis).

13. Eccentric Training

    • Controlled lengthening contractions to promote tendon remodeling.

14. Aerobic Conditioning

    • Low-impact activities (cycling, swimming) to support overall fitness without overloading entheses.

15. Proprioceptive Training

    • Balance and coordination drills to optimize load distribution across entheses BMJ Arthritis Research & Therapy.

Mind-Body Therapies

16. Mindfulness-Based Stress Reduction (MBSR)

    • Description: Eight-week program of meditation and gentle yoga.

    • Purpose: Reduce pain perception and improve coping.

    • Mechanism: Modulates brain regions involved in pain processing and stress response PMC.

17. Yoga

    • Description: Structured asanas, breathing, and meditation.

    • Purpose: Enhance flexibility, strength, and stress management.

    • Mechanism: Integrates physical postures with relaxation to reduce pain and improve function PMC.

18. Tai Chi/Qigong

    • Gentle martial-arts–style movements to promote mind-body awareness and joint health.

Educational Self-Management

19. Patient Education Sessions

    • Knowledge about enthesitis, load management, and joint protection strategies.

20. Activity Pacing & Goal Setting

    • Structured plans to gradually increase activity without overloading entheses Wikipedia.

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Key Drugs

Management often requires pharmacotherapy targeting inflammation and immune modulation:

1. Ibuprofen (NSAID)

   • Dosage: 400–800 mg TID

   • Timing: With meals

   • Side Effects: GI upset, renal impairment NICE.

2. Naproxen (NSAID)

   • Dosage: 250–500 mg BID

   • Side Effects: Dyspepsia, headache NICE.

3. Diclofenac (NSAID)

   • Dosage: 50 mg TID

   • Side Effects: Elevation of liver enzymes, cardiovascular risk NICE.

4. Indomethacin (NSAID)

   • Dosage: 25 mg TID

   • Side Effects: CNS effects (headache, dizziness) NICE.

5. Triamcinolone Hexacetonide (IM injection)

   • Dosage: 20–40 mg once per inflamed enthesis

   • Side Effects: Local pain flare, tendon weakening JRheum.

6. Methotrexate (Conventional DMARD)

   • Dosage: 7.5–25 mg weekly

   • Side Effects: Hepatotoxicity, cytopenias JRheum.

7. Sulfasalazine (Conventional DMARD)

   • Dosage: 500 mg BID → 2 g/day

   • Side Effects: GI intolerance, rash JRheum.

8. Adalimumab (TNF inhibitor)

   • Dosage: 40 mg SC every other week

   • Side Effects: Infections, injection-site reactions BMJ Arthritis Research & Therapy.

9. Etanercept (TNF inhibitor)

   • Dosage: 50 mg SC weekly

   • Side Effects: Reactivation of latent TB, demyelinating disease BMJ Arthritis Research & Therapy.

10. Secukinumab (IL-17A inhibitor)

    • Dosage: 150 mg SC at weeks 0,1,2,3,4, then monthly

    • Side Effects: Candidiasis, neutropenia BMJ Arthritis Research & Therapy.

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Dietary Molecular Supplements

Adjunctive supplements may support anti-inflammatory balance:

1. Glucosamine Sulfate 1 500 mg/day – promotes cartilage matrix production.

2. Chondroitin Sulfate 1 200 mg/day – inhibits degradative enzymes.

3. Omega-3 Fatty Acids 1–3 g/day – shift eicosanoid profile toward anti-inflammatory mediators.

4. Curcumin 500–2 000 mg/day – NF-κB pathway inhibition Health.

5. Boswellia Serrata 300 mg TID – 5-lipoxygenase inhibition EatingWell.

6. Ginger Extract 500 mg BID – COX and LOX inhibition.

7. Hydrolyzed Collagen 10 g/day – supplies amino acids for tendon repair.

8. MSM (Methylsulfonylmethane) 2 g/day – sulfation support for connective tissue.

9. Vitamin D₃ 1 000–2 000 IU/day – immunomodulation.

10. Vitamin C 500–1 000 mg/day – cofactor for collagen synthesis.

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Advanced Regenerative & Biologic Therapies

1. Bisphosphonates (Alendronate) 70 mg weekly – inhibit osteoclast-mediated bone resorption, may reduce enthesis bone changes.

2. Zoledronic Acid 5 mg IV annually – potent anti-resorptive.

3. Platelet-Rich Plasma (PRP) 3–5 mL per injection monthly × 3 – delivers growth factors to promote healing PubMed.

4. Autologous Conditioned Serum weekly × 6 – anti-inflammatory cytokine enrichment.

5. Hyaluronic Acid Viscosupplementation 2–4 mL weekly × 3 – lubricates peri-enthesis areas, reduces friction PubMed.

6. Mesenchymal Stem Cell (MSC) Injections ~1–2×10⁶ cells per site – secrete trophic factors, modulate inflammation, and promote matrix remodeling PMC.

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Surgeries

Surgery is reserved for refractory cases after ≥ 6 months of conservative care AOA Orthopedic Specialists.

1. Endoscopic Achilles Debridement

   • Procedure: Arthroscopic removal of damaged tendon and calcifications.

   • Benefits: Faster recovery, less wound complications Resurgens Orthopaedics.

2. Achilles Tendon Lengthening (Percutaneous/Z-Plasty)

   • Procedure: Tenotomy or Z-shaped cuts to elongate tendon.

   • Benefits: Reduces tension at enthesis, improves dorsiflexion Resurgens Orthopaedics.

3. Plantar Fascia Release

   • Procedure: Partial cut of medial one-third plantar fascia, endoscopic or open.

   • Benefits: Relieves tension in cases of insertional enthesitis (plantar heel) Resurgens Orthopaedics.

4. Percutaneous Ultrasonic Tenotomy (Tenex Procedure)

   • Procedure: Ultrasound-guided percutaneous removal of diseased tissue.

   • Benefits: Minimally invasive, rapid return to activity Verywell Health.

5. Gastrocnemius Recession

   • Procedure: Lengthening of gastrocnemius aponeurosis to unload Achilles enthesis.

   • Benefits: Improved ankle dorsiflexion, reduces insertional stress Wikipedia.

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Prevention Strategies

1. Perform regular stretching of tendon–muscle units.

2. Strengthen surrounding musculature (e.g., eccentric heel raises).

3. Gradually increase activity intensity and duration.

4. Wear supportive, well-fitting footwear with adequate cushioning.

5. Avoid running or jumping on hard surfaces.

6. Maintain healthy body weight to reduce enthesis load Wikipedia.

7. Incorporate cross-training (cycling, swimming).

8. Warm up thoroughly before exercise.

9. Use orthotics or heel lifts when indicated.

10. Address biomechanical issues (e.g., overpronation) with professional assessment.

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When to See a Doctor

• Duration: Pain persisting > 6 weeks despite self-care.

• Severity: Night pain, inability to bear weight.

• Signs of Complication: Redness, warmth, fever, sudden functional loss.

• Systemic Symptoms: Joint swelling elsewhere, psoriasis, inflammatory bowel disease.
  Prompt evaluation ensures early intervention and prevents chronic enthesis damage Wikipedia.

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Do’s & Don’ts

Do:

1. Rest and apply ice during flares.

2. Follow a graded exercise program.

3. Use orthoses as directed.

4. Maintain overall fitness with low-impact activities.

5. Communicate symptoms openly with your healthcare team.

Don’t:

1. Ignore persistent pain—seek care.

2. Resume full activity immediately after pain relief.

3. Overstretch inflamed enthesis.

4. Use unsupervised heavy loading or plyometrics.

5. Rely solely on corticosteroid injections—avoid overuse.

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FAQs

1. What is fibrocartilaginous enthesitis?
   Inflammation of a fibrocartilaginous tendon insertion characterized by pain and structural changes Wikipedia.

2. What causes it?
   Overuse, mechanical stress, and autoimmune processes (e.g., spondyloarthritis) Frontiers.

3. What are common symptoms?
   Localized pain, tenderness at the bone insertion, swelling, and stiffness.

4. How is it diagnosed?
   Clinical exam, ultrasound/MRI revealing enthesis thickening, Doppler signal, and bone erosions.

5. Can exercise worsen it?
   Improper loading can exacerbate enthesitis; graded, guided exercise is key BMJ Arthritis Research & Therapy.

6. Are NSAIDs effective?
   Yes, first-line for symptom relief, but long-term use requires monitoring for side effects NICE.

7. When are injections indicated?
   Persistent focal pain after NSAIDs and physiotherapy; ultrasound-guided triamcinolone is preferred.

8. Do supplements help?
   Some may offer modest benefits (glucosamine, omega-3, curcumin) but evidence is limited Health.

9. Is surgery always needed?
   No—only for refractory cases after ≥ 6 months of comprehensive conservative care AOA Orthopedic Specialists.

10. Can enthesitis recur?
    Yes, especially if underlying systemic disease or mechanical risk factors persist.

11. Are biologic drugs helpful?
    TNF and IL-17 inhibitors can provide significant relief in autoimmune-associated enthesitis BMJ Arthritis Research & Therapy.

12. What role does diet play?
    A balanced anti-inflammatory diet may support overall management, but no specific diet cures enthesitis.

13. Is enthesitis chronic?
    It can become chronic, especially if systemic disease is uncontrolled.

14. Can physical therapy cure it?
    PT manages symptoms and function; it’s part of a multimodal plan, not a standalone cure JRheum.

15. What is the long-term outlook?
    With appropriate management, many patients achieve pain relief and return to normal activity levels.

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.

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