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Table 1 Outcome of arthritis in osteoclast-free mouse models

From: The role of osteoprotegerin in arthritis

 

Pettit et al. [11]

Redlich et al. [14]

Arthritis model

K/BxN (serum transfer)

hTNF transgenic

Osteoclast-deficiency model

RANKL-/-

c-fos-/-

Mechanism of arthritis

Immune complex driven

Cytokine overexpression

Mechanism of bone pathology

Stromal cell defecta

Bone marrow cell defectb

Effect on inflammation

No

No

Effect on cartilage damage

Partlyc

No

Effect on bone erosion

Yes

Yes

Presence of osteoclasts

No

No

  1. a Absent receptor-activator of nuclear factor kappa B ligand (RANKL) expression on stromal cells blocks osteoclastogenesis. Osteoclast precursor cells are normal and express receptor-activator of nuclear factor kappa B (RANK). b Blockade of osteoclastogenesis is downstream of RANK and is limited to the osteoclast lineage. RANKL expression by stromal cells is normal. c 0–50% inhibition of cartilage damage; positive effects predominantly found at the forefoot.