what kind of fibers do they have?
Tendons have type 1 collagen fibers
1. Tendon made up of FASCICLES. Fasciles move past each other longitudinally like aligned spaghetti.
2. Fascicles are enwrapped in ENDOTENONS and are made up of FIBRILS.
Endotenons contain blood vessels in between fascicles.
3. Collagen fibrils follow a zig zag waveform in longitudinal orientation forming a CRIMP. Safety mechanisms-when start stretching tendon the fibrils straighten when they stretch Fibrils are made up of SUB FIBRILS
4. Sub-fibrils are made up of MICO FIBRILS which contain TROPOCOLLAGEN.
Inner Synovial Sheath
Tendon in the Synovial Sheath.
Tendon in the Eptionon
Fibroblasts: Mesenchymal Cells. Produce fibrous connective tissue.
Synthesize and degrade all of the collagenous and non collagenous matrix (proteoglycans
Adult 75% of mass is type 1 Collagen (Type 4 in BM and Type 2 in Cartilage)
Tenoblasts are more active and numerous in young animals .
As tendon gets older gets more tenocytes and less tenoblasts become less active because tenocytes are less active than tenoblasts.
Tenocytes have a long nucleus.
Tenocytes are linked by gap junctions.
Superficial digital flexor tendon injury.
Age is a risk factor for injury.
Usually occurs spontneously during exercise. A healthy tendon doesn't rupture.
Therefore, the tendon must have a previous accumulation of damage= MICRODAMAGE which is subclinical.
Early Microdamage in the SDFT:
Increase in type 1 tenocytes
Decrease in gap junction communication
Decrease in crimp angle
Decrease in crimp angle
Decrease in collagen fibril diameter
Why is SDFT prone to injury?
It store kinetic and potential energy as elastic energy and act as a spring.
Kinetic --> Potential --> Elastic --> Biological spring activity
Energy storing tendons have low mechanical safety margins.
SDFT is loaded before other digital tendons/ ligaments therefore it is bearing all the weight for a fraction of a second.
Cells involved in Tendon repair:
- Endotonon and Epitenon: Intrinsic repair
-Extrinisic repair: Tendon has no internal ability and requires adhesions and extra tendonous blood supply.
Dramatic hypertrophy of the endotenon by both vascular and fibroblastic elements.
The major problems in Tendon healing:
Fascicles stuck together and destoryed by scar tissue, Do not regenerate.
Scar tissue persists
Inflammatory cells persist in the endotenon.
For region of tendons with overlying snyovial sheats, there may be a secondary synovitis.
White to blue grossly
Thickest in young animals at and at sites of maximal weight bearing.
At margins merges with periosteal surface lined by fibrous tissue that is contiguous with the synovial membrane.
No Nerves,blood, or lymphatic vessels
Gets its nutrition from diffusion of synovial fluid and subchondral vessels.
Chondrocytes are NOT mitotically active and have poor regeneration capacities.
Mainly type 2 collagen.
Cartilage layers and functions:
Superficial layer: resists shearing forces. (NOT CALCIFIED)
Middle layers: function in shock absorption. (NOT CALCIFIED)
Tidemark: boundary between uncalcified articular cartilage and the calcified cartilage.
Calcified Cartilage: attaches articular cartilage to bone by its irregular interlocking interfaces.
Cartilage --> Calcified Cartilage --> Bone
Injury is not painful unless subchondral bone or synovium involved.
Subchondral bone is below the aritcular cartilage at the end of bones on top of the epiphysis that resemebles the epiphysis.
Injury to cartilage does not participate in the inflammatory response however inflammation can affect it if the inflammation occurs in the synovium, subchondral bone, or growth cartilage.
As in the tendon, Repetitive stress, ageing can damage both the matrix and the chondrocytes leading to inappropriate cellular responses, chondrocyte death, and injury. (microdamage)
Disruption of collage, proteoglycans, and their interactions with each other.
Cartilage Injury & Repair:
Limited response to injury and minimal capacity for repair.
If proteoglycans are lost collagen fibers condense and fray = FIBRILLATION accompanied by erosion.
Fibrillation is a disrupted surface (not smooth) perpendicular to the joint surface (up and down)
Erosion does not penetrate to subchondral bone therefore.
Subsequen to fibrillation and erosion is --> NECROSIS OF CHONDROCYTES. (hypocellularity)
Very Limited regeneration of chondrocytes - usually ineffective.
does not penetrate subchondral bone.
Subsequent to fibriallation and erosion is Necrosis of chondrocytes (hypocellularity)
Limited regerative hyperplasia of chondroctyes (ineffective)
Full thickness loss to bone.
Usually undergoes metaplasia to fibrocartilage.
The now exposed subchondral bone develops increased density due to increase mechanical use. = eburnation
Increased density of subchondral bone develops due to Increased load on the bone due to loss of cartilage usually from ulceration.
Degenerative Joint Disease (DJD)
1. Chondromalacia (softening)- injury causes loss of proteoglycans causing collagen fibers to condense and fry causing
2. Fibrillation and erosion
Formation of osteophytes (multiple bony outgrowths/ spurs)
Growth of the osteophytes is initiated by mechanical instability of the joint and or inflammatory cytokines.
Osteophytes do not keep growing however they persist meaning they never regress.
They can form within the joint cavity or from periosteum at junction with joint capsule.
Seen with chronic inflammatory diseases.
Happens with chronic infectious synovitis or immune mediated diseases. (rheumatoid arthritis)
So the synovium becomes severely inflammed due to infectious synovitis, immune mediate disease or rheumatoid arthritis. Then, pannus develops.
Pannus is a fibrovascular tissue arising from synovium and spread over the articular cartilage. (This occurs early in its formation)
Later in (once pannus is formed): Macrophages and collagenases invade and destroy cartilage and subchondral bone.
A disease of growth plate cartilage:
A group of lesions in young animals
Often bilaterally symmetrical
Focal or multifocal failure of endochondral ossification. ( no mineralization of the cartilage in these areas)
Involves metaphyseal growth plate and articular epiphyseal complex.
Metaphysis region- no ossification due to accumulation of viable hypertrophic chondrocytes
AE complex- no ossification due to necrosis of epiphyseal cartilage.
The growing cartilage will be vascular (only in young cartilage remember mature articular cartilage is not vascular)