Table 1

Outcome of arthritis in osteoclast-free mouse models

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 defect^a

Bone marrow cell defect^b

Effect on inflammation

No

No

Effect on cartilage damage

Partly^c

No

Effect on bone erosion

Yes

Yes

Presence of osteoclasts

No

No

^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.

Schett et al. Arthritis Res Ther 2003 5:239   doi:10.1186/ar990