Flashcards in Tissue Injury and Repair 5 Deck (27)
Fascicle- largest subunit of tendons. ~1mm diameter, hexagonal cross section.
Move past each other.
Crimp- 'safety mechanism'
Fascicle is made up of zig zag fibrils.
Each fibril is made of stacked collagen in a quarter stagger arrangement.
Each collagen molecule is a triple helix.
Collagen type I, II, III.
Type I mainly seen in adults.
Type III- smaller fibrils.
Produce matrix- mostly (75%) type I collagen, also glycoproteins. 7
"Synthesise and degrade all of the collagenous and non collagenous matrix"
less active than tenoblasts (more numerous in younger animals, tenoblasts become tenocytes as animal ages)
Linked by gap junctions and adherence junctions in to a network.
Connective tissue between fascicles.
Contains blood vessels to supply fascicles, as they do not contain blood vessels.
Tenocytes extend processes that surround fibrils and attach them, so can sense when contraction/relaxation occurs.
Tendon stem/progenitor cells are present. They are thought to be round.
SUPERFICIAL DIGITAL FLEXOR TENDON
Most studied and understood tendon.
Age is a risk factor.
Overuse injury causes spontaneous tendon rupture during exercise- "a healthy tendon doesn't rupture"- the tendon is already weakened due to MICRODAMAGE.
Damage is subclinical, but accumulates, eventually becoming clinical.
MICRODAMAGE IN THE SDFT
Caused by exercise and/or ageing:
AGEING: Decreased cellularity, increased type I tenocyte number and length.
Decreased gap junction communication.
Decreased core crimp angle over 10 years.
EXERCISE: Decreased crimp angle in horses UNDER 10 years, decreased collagen fibril diameter, decreased glycosaminoglycan content.
Many exercise induced changes appear to represent premature aging.
RED CORE LESION
More advanced damage in SDFT.
No clinical signs or swelling. Often found incidentally at PM, cen be seen on ultrasound.
more TYPE III collagen- smaller fibres, weaker -> injury prone.
Subclinical, but horses with red core lesions have a much higher chance of future tendon rupture.
WHY IS THE SDFT PRONE TO INJURY?
Stores kinetic and potential energy as elastic energy- BIOLOGICAL SPRING- stored energy is returned to horse as foot leaves ground. Less muscle work is required- 36% energy saving during gallop.
Muscle acts to dampen high frequency oscillations in the limb.
Tendons undergo a lot of stretch to save energy- they work almost to the point of failure during gallops- LOW MECHANICAL SAFETY MARGIN.
5-10% of energy is lost as heat- core temperature of SDFT can reach 45c on gallop.
SDFT is loaded slightly before other tendons (DDFT); it takes the entire weight of the horse.
*Gait should be taken in to account when assessing ligaments eg. trotters switch their weight to the suspensory ligament, so this is more prone to injury than the SDFT.
EQUINE SDFT- "THE PERFECT STORM"
Susceptible population, few cells, inactive (no turnover of collagen once mature), linked together, ageing.
Any cell death or dysfunction is significant.
The tendon cells may play an active role.
CAUSES: Ageing, hypoxia, overstress, understress- matrix breakdown, compression, hyperthermia.
NATURE OF DYSFUNCTION: Type III collagen, matrix metalloproteinases (MMPs)- made in normal tendon but increase in injury and start to break down matrix, inflammatory mediators.
HUMAN EQUIVALENT OF SDFT?
Similar in terms of function, injury susceptibility and pathology.
CLINICAL TENDON INJURY
Injury response is same as other tissues, but faster.
Acute (inflammatory) phase
-> Subacute (proliferation) phase- enlargement, neovascularisation, fibroplasia, inflammation.
-> Chronic (remodelling and maturation) phase- >3 months, still enlarged, thickened paratenon, scar tissue.
CELLS INVOLVED IN TENDON REPAIR
-Fibroblastic cells- Endotenon and epitenon provide the most repair- INTRINSIC.
EXTRINSIC REPAIR- tendon has no internal ability and requires adhesions and extratendonous blood supply (probably a variable combination).
-Tenocytes- in peri-lesional tissue
-Stem cells (?)
There is dramatic hypertrophy of the endotenon by vascular and fibroblastic elements.
MAJOR PROBLEMS IN TENDON HEALING
-Fascicles are stuck together by scar tissue and not regenerated, so cannot move past each other and store elastic energy.
-Scar tissue persists- increased Type III collagen for 14 months +. Reinjury is much more likely at the junction between normal and scar tissue.
-Much more cellular than normal tissue.
Inflammatory cells and blood vessels persist in endotenon- linked with ongoing pain in humans.
Older horses are less able to resolve this.
TENDONS WITH OVERLYING SYNOVIAL SHEATHS
Secondary synovitis (swollen/oedematous sheath with villus like projections) may be seen.
White to blue grossly.
Thickest in young animal and at sites of maximal weight bearing.
Merges with periosteal surfaces and synovium at margins.
Avascular, denervated, alymphatic.
Injury is not painful unless synovium or bone are involved.
Nutrition is via DIFFUSION from synovial fluid and subchondral vessels.
Chondrocytes are not mitotically active and have poor regenerative ability.
Collagen mainly Type II
Decreased cellularity, turnover of cells and collagen.
LAYERS OF CARTILAGE
-SUPERFICIAL LAYER resist shearing forces
-MIDDLE LAYERS function in shock absorption
-TIDEMARK- boundary between uncalcified articular cartilage and calcified cartilage
-CALCIFIED CARTILAGE attaches articular cartilage to bone with it's irregular interlocking surface.
Not painful unless subchondral bone or synovium is involved.
Does not participate in inflammatory responses, but is affected by synovial/subchondral bone/growth cartilage inflammation.
Sterile injury can be a consequence of trauma, joint instability, lubrication failure. eg. synovial pathology.
Resists neoplastic inflammation- tumours do not penetrate.
As in tendon, repetitive stress can damage both the matrix and chondrocytes, leading to inappropriate cellular responses and accumulation of microdamage.
CARTILAGE INJURY AND REPAIR
Minimal response to injury and minimal capacity for repair.
If proteoglycans are lost, causes collagen fibres to condense and fray.
Clefts and fissures appear in vertical axis (perpendicular to joint surface)
Fibrillation is accompanied by erosion.
Complete loss of cartilage (ulceration) is accompanied by bony sclerosis at the area of loss due to increased mechanical use.
Chondromalacia and fibrillation.
Does not penetrate to subchondral bone.
Persistent- doesn't heal or progress.
Subsequent to fibrillation and erosion, NECROSIS of chondrocytes is seen (hypocellularity)
Limited regenerative hyperplasia of chondrocytes is seen, but this is almost always ineffective.
Full thickness loss of cartilage.
Loss is filled with vascular fibrous tissue.
Often undergoes metaplasia to fibrocartilage, but rarely hyaline cartilage.
Exposed subchondral bone develops increased density due to increased mechanical use- EBURNATION.
DEGENERATIVE JOINT DISEASE
CHONDROMALACIA -> EROSION AND FIBRILLATION -> ULCERATION
-Often see formation of periarticular osteophytes- multiple bony outgrowths/spurs.
-Initiated by mechanical instability of joint and/or inflammatory cytokines.
-Osteophytes do not grow continuously but persist once formed.
-Osteophytes can form within the joint cavity (perichondrium) or form periosteum at junction with joint capsule.
-Often see secondary synovial inflammation and hyperplasia.
Happens in chronic infectious synovitis or immune mediated disease.
INFLAMMATORY or IMMUNE MEDIATED.
Fibrovascular and inflammatory tissue.
Severe synovial inflammation produces tissue, which starts to spread over articular surface and penetrates.
Macrophages and collagenases destroy the cartilage.
Entire joint may become fused.
CARTILAGE OF THE GROWTH PLATE
Bone being deposited.