Rheumatoid Arthritis, JointsSlide no. 179

By: Abel, Joriz Kevin Abergas, Unica May

Etiology

Cause remains unknown Factors that contribute to development,

progression and chronicity : Genetic Susceptibility▪ HLA-DRB1: shared epitope is specific binding site of

arhritogens▪ PTPN22: activation and control of inflammatory cells

Environmental arthritogens▪ Microbial agents▪ Citrullinated proteins

Autoimmunity▪ Rheumatoid factors

Genetic susceptibilityArthritogens

Activation of CD4+ helper T cells

Release of cytokinesINF-γ & IL-17

Stimulation of synoviocytes and macrphages

Production of pro-inflammatory molecules:IL-1, 6, 23, TNF, PGE2, NO,GF, GM-CSF, TGF-β

Increase production of

cartilage matrix metalloproteina

ses

Stimulation of osteoclastogenesis

and osteoclast activity

Synoviocytes up-regulate vascular

cell-adhesion molecule

Edematous, hyperplastic, sticky synovium

Pannus formation and resorption of the adjacent bone

PATHOGENESIS

Gross Morphology

Histologic Morphology

Inflammatory infiltrate composed of lymphoid aggregates

Increased vascularity

Accumulation of neutrophils

Pannus formation

Clinical Significance

Manifestations: Mild general aching and stiffness Inflammation may be apparent first in the wrists

and fingers Joints appear red and swollen and often very

sensitive to touch as well as painful Joint stiffness “burned out” Systemic signs are marked during exacerbations

and inclued fatique, anorexia, mild fever, lymphadenopathy and genralized aching

Clinical Significance

Complications: Effects on the Skin▪ Rheumatoid Nodules

Eye Complications▪ Inflammation of the episclera▪ Scleritis▪  Sjogren's syndrome

Effects on Heart and Blood Vessels  Pericardial Effusion Pericarditis Myocarditis

Diseases of the Blood and Blood-Forming Cells Anemia Felty's syndrome

Lung Problems

Emotional Effects

Susceptibility to Infection