Extracellular matrix26, 76, 77, 120, 121, 122, 123
|
Degradation of the proteoglycans: Less fluid attracted to nucleus pulposus |
Degradation of the proteoglycans: Less fluid attracted to the articular cartilage |
Decrease in intradiscal pressure |
Decrease in intra‐articular pressure |
Shift to collagen type I: Nucleus pulposus becomes more fibrous |
Shift to collagen type I: Articular cartilage becomes more fibrous |
Biomechanics48, 121, 124
|
Reduced disc height |
Reduced joint space |
Increase in shear stresses |
Increase in shear stresses |
Less resistive to compressive loads |
Less resistive to compressive loads |
Cells95, 96, 97, 98, 99, 100
|
Inflammatory mediators: Production of catabolic factors |
Inflammatory mediators: Production of catabolic factors |
Catabolism by the chondrocyte‐like cells: Degradation of ECM |
Catabolism by the chondrocytes: Degradation of ECM |
Caused by 58, 74, 75, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94
|
Local inflammation |
Systemic inflammation by |
Diabetes |
Local inflammation |
Systemic inflammation by |
Diabetes |
Obesity |
Obesity |
Smoking |
Smoking |
Mechanical overloading |
Mechanical overloading |
Inflammatory factors93, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 125, 126, 127
|
TNF‐α and IL‐1β |
TNF‐α and IL‐1β |
MMP 1–3, MMP 7–10, and MMP 12–14 |
MMP 1‐3 and 7–14 |
ADAMTSs 4 and 5 |
ADAMTSs 4 and 5 |
TIMP 1–3 |
TIMP 1–3 |
Clinical symptoms12, 13, 14, 128
|
Pain |
Pain |
Dysfunction |
Dysfunction |
Morning stiffness |
Morning stiffness |
Radiological findings4, 15, 129, 130
|
Formation of cysts and osteophytes |
Formation of cysts and osteophytes |
Loss of joint space |
Loss of joint space |
Subchondral sclerosis |
Subchondral sclerosis |
Adjacent structures involved25, 74, 81, 131
|
Vertebrae |
Bone of tibia and femur |
Facet joints |
Meniscal tears |
Modic changes |
Synovitis |
Nerve roots, ligaments and muscles |
Nerve roots, ligaments and muscles |