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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.