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Related Concept Videos

Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
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Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Amyloid Fibrils03:03

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Microsporidia are a group of obligate intracellular fungi that were initially classified as protists but were later reclassified based on phylogenetic, molecular, and structural evidence linking them to the Chytridiomycota. These unicellular, non-motile organisms are highly specialized parasites that infect a wide range of animal hosts, including humans. They have evolved extensive genomic and metabolic reductions, making them highly dependent on their hosts for survival.Morphology and Genomic...
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Related Experiment Video

Updated: May 27, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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Freiberg's disease.

Rebecca A Cerrato1

  • 1Institute for Foot and Ankle Reconstruction, Mercy Medical Center, 301 St Paul Place, Baltimore, MD 21202, USA. rcerrato@mdmercy.com

Foot and Ankle Clinics
|November 29, 2011
PubMed
Summary

Freiberg’s disease, a rare metatarsal head disorder, has multifactorial causes including trauma. Initial treatment focuses on conservative methods, while surgery addresses progression or later-stage issues.

Area of Science:

  • Orthopedics
  • Foot and Ankle Surgery
  • Sports Medicine

Background:

  • Freiberg’s disease is an uncommon disorder affecting the metatarsal head.
  • Its etiology is multifactorial, with trauma and circulatory issues playing significant roles.

Purpose of the Study:

  • To review the current understanding and management strategies for Freiberg’s disease.
  • To discuss conservative and surgical treatment options, including newer regenerative techniques.

Main Methods:

  • Literature review of Freiberg’s disease etiology, pathophysiology, and treatment modalities.
  • Categorization of surgical approaches into corrective and sequelae-addressing procedures.

Main Results:

  • Conservative treatment, emphasizing stress relief and offloading, is the standard initial approach.

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  • Surgical options aim to correct the underlying pathology or manage advanced disease symptoms.
  • Osteochondral transplantation represents a newer strategy for cartilage restoration.

    • Conclusions:

    • Effective management of Freiberg’s disease requires a tailored approach based on disease stage.
    • Conservative measures are primary, with surgical intervention reserved for specific indications.
    • Emerging techniques like osteochondral transplantation offer potential for cartilage repair.