Bone

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Bone is a scaffold it bears weight and occasionally gets infected.

Tumours often spread to bone and occasionally arise in bone. Bone tumours are dealt with in the bone tumours article.

Normal

  • Normal bone has osteocytes.
    • If the osteocytes are missing... the bone is dead.
  • Osteoblasts - make bone.
  • Osteoclasts - destroy bone.

Memory device: 'b' before 'c'.

Hyperostosis frontalis interna

  • Extra-thick frontal bone.[1]
  • No clinical significance -- just has to be recognized as a "nothing".

Bone marrow

  • Fat content (%) ~= age (in years)[2]
    • e.g. 60 year old will have 60% fatty replacement.
  • Should see three cell lines.
    • The cell lines:[3]
      • Erythroid (red cells),
      • Myeloid (white blood cells),
      • Megakaryocytic (platelets).

Note: Lymphocytes are considered separately and typically spared in bone marrow failure.[4]

Identifying the lines:[5]

  1. Megakaryocytes:
    • Big cells ~ 3x the size of a RBC.
  2. Normoblasts (RBC precursors):
    • Hyperchromatic, i.e. blue, nucleus.
  3. Myeloid line:
    • Granules.
    • Reniform nucleus, i.e. kidney bean shaped nucleus.

Images:

Organization

  • Mature hematopoeitic cells at the centre (distant from bone).
  • Immature hematopoeitic cells adjacent to the bone.

Infectious

Osteomyelitis

General

  • Hematogenous - often in children.
  • Direct entry (skin defect) - adults with diabetes.

Microscopic

  • PMNs.

Chronic osteomyelitis

  • Plasma cells.
    • May be sterile, i.e. no organisms.

Bone tumours

This is a big topic. It is dealt with in a separate article.

The bone tumour article covers tumour mimics, e.g. brown cell tumour.

Fractures

This is dealt with in the forensic pathology article.

Others

The following is a collection of weird stuffs.

Myositis ossificans

  • AKA fibro-osseous pseudotumour of digits.[6]

Epidemiology:

  • Young people.
  • History of trauma.

Microscopic

Features:[6]

  • High cellularity.
  • Low mitotic activity.
  • No atypical mitoses.
  • No hyperchromasia.

Other features:[7]

  • Low power diagnosis:
    • Lesion is well-circumscribed.
    • Normal muscle is adjacent to the lesion.

Paget disease of the bone

General

Classically divided into three phases:[8][9]

  1. Lytic (predominantly osteoclasts).
  2. Mixed lytic (osteoclastic) and blastic (osteoblastic).
  3. Sclerotic (burned-out).

Clinical:

  • Elevated ALP.

Microscopic

Features:[8]

  • Bone matrix has jigsaw-puzzle like pattern.
    • Jigsaw-puzzle pieces each ~ 100-500 micrometres in size (largest dimension).
  • Increased osteoclast activity.
    • Osteoclast = macrophage that resorbs bone matrix.

Images:

See also

References

  1. URL: http://radiopaedia.org/articles/hyperostosis_frontalis_interna. Accessed on: 29 September 2010.
  2. IAV. 26 Feb 2009.
  3. http://emedicine.medscape.com/article/199003-overview
  4. http://emedicine.medscape.com/article/199003-overview
  5. http://upload.wikimedia.org/wikipedia/commons/6/69/Hematopoiesis_%28human%29_diagram.png
  6. 6.0 6.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 607. ISBN 978-0781765275.
  7. IAV. 9 December 2010.
  8. 8.0 8.1 URL: http://emedicine.medscape.com/article/311688-overview. Accessed on: 25 December 2010.
  9. URL: http://radiopaedia.org/articles/paget-disease-of-bone-1. Accessed on: 25 December 2010.