SEARCH RESULTS FOR: Costochondritis

Costochondritis

Costochondritis: Pathogenesis and clinical findings Systemic infection originating in upper respiratory tract (commonly Staphylococcus aureus and Streptococcus bacterial infections) Infection spreads through blood to ribcage and chest wall Age-related degeneration of cartilage within ribcage joints Immune cells present in joints secrete proinflammatory cytokines Cytokines sensitize nociceptors (pain receptors) in joints Repetitive trauma or strain to chest wall muscles (e.g. chronic cough, chest wall injury, overexertion of chest wall muscles) Excessive stretch and tearing of ribcage cartilage and ligaments Autoimmune disease (e.g. rheumatoid arthritis) Antigen presenting cells display self-antigens to CD4+ T cells Mechanical stimuli (e.g. Damaged cells release cytokines Pathogens activate immune cells at site of stretch) activate nociceptors that recruit immune cells inflammation Costochondritis Benign inflammation of the ribcage (costal) cartilage, particularly at the costosternal junctions (connection between sternum and cartilage) and the costochondral junctions (connection between the cartilage and rib) Authors: Michelle J. Chen Reviewers: Raafi Ali Yan Yu* Gerhard Kiefer* * MD at time of publication Cartilage, ligament, or muscle injury Presence of foreign pathogen in costal cartilage Injury or pathogen activates inflammatory cascade in the ribcage cartilage Immune cells proliferate so that they exceed the available space in the cartilage matrix of the ribcage Cartilage swelling compresses intercostal nerves Compression acts as a mechanical stimulus to activate nociceptors Sharp, localized pain reproducible upon palpation over ribcage Immune cells secrete cytokines Cytokines activate nociceptors so that they become more sensitive to mechanical stimuli Muscle or ligament stretch from normal use activates sensitized nociceptors Pain increases with inspiration or cough Natural resolution of inflammation over time Macrophages phagocytose apoptotic cells (immune and cartilage cells) and cellular debris Immune cells release factors that degrade proinflammatory cytokines Fewer cytokines reduce immune cell recruitment into costal cartilage Pain usually self-resolves Immune cells release lipid molecules that bind to the same cells (autocrine signaling) to inhibit further production of inflammatory cytokines and chemokines Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Apr 29, 2024 on www.thecalgaryguide.com