Rheumatoid Arthritis (RA)
At a microscopic level, joint cartilage destruction and bone loss are associated with an inflamed synovial lining that results from chronic activation of both innate and adaptive immune cells and stromal cells in the joint, leading to RA. CrownBio’s platform consists of preclinical models with diverse mechanisms that capture many of the key characteristic clinical and pathologic features of RA. These models determine efficacy and response to treatment and improve selection of your next qualified lead agent.
Collagen Antibody-Induced Arthritis Mouse Model – CAIA
RA is induced through administration of commercially available antibodies targeting Type II collagen and results in rapid onset of disease.
Collagen-Induced Arthritis Mouse Model – CIA
DBA/1 mice are immunized with Type II collagen and boosted with IFA. Peak disease occurs 8-15 days post IFA boost.
- Swollen joint count
- uCT to quantitate joint bone damage
- Assessment of inflammatory mediators/cytokines
- Histopathological assessment
CAIA Model + Dexamethasone
Representative Forepaw Histology Photomicrographs
Non-lesioned paw. A distal phalangeal bone (P), carpal bone (C), and proximal interphalangeal joint (J) are indicated.
Marked inflammation (*) of the intra- and peri-articular tissues, affecting the interphalangeal joints (phalangeal bone, P) and carpal (C) joints is noted. Cartilage damage (black arrows), bone resorption (black arrowheads), pannus (blue arrowheads), and periosteal new bone (NB) are indicated.
Forepaw lacks lesions associated with arthritis. Interphalangeal joint (J), proximal phalangeal bone (P), and carpal bone (C) are indicated.