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 bone

Bone

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

Memory device: 'b' before 'c'.

Bone marrow

  • Fat content (%) ~= age (in years)[1]
    • e.g. 60 year old will have 60% fatty replacement.
  • Should see three cell lines.
    • The cell lines:[2]
      • Erythroid (red cells),
      • Myeloid (white blood cells),
      • Megakaryocytic (platelets).

Note: Lymphocytes are considered separately and typically spared in bone marrow failure.[3]

Identifying the lines:[4]

  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.

Benign variants

Hyperostosis frontalis interna

  • Extra-thick frontal bone.[5]
  • No clinical significance -- just has to be recognized as a "nothing".

Infections

Osteomyelitis

General

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

Microscopic

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]

General

Epidemiology:

  • Young people.
  • History of trauma - typically.
  • Extremities - digits (fingers, toes).

Notes:

  • Histologically "worrisome" (for malignancy) - due to high cellularity.[6]

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 - key feature.

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. IAV. 26 Feb 2009.
  2. http://emedicine.medscape.com/article/199003-overview
  3. http://emedicine.medscape.com/article/199003-overview
  4. http://upload.wikimedia.org/wikipedia/commons/6/69/Hematopoiesis_%28human%29_diagram.png
  5. URL: http://radiopaedia.org/articles/hyperostosis_frontalis_interna. Accessed on: 29 September 2010.
  6. 6.0 6.1 6.2 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.