Chapter 84 - Diagnosis and Management of Tendon and Ligament Disorders Flashcards
1
Q
What is the primary component of the extracellular matrix in tendons by wet weight?
A
Water (about 65%).
2
Q
What type of collagen constitutes the majority of tendon collagen?
A
Type I collagen (about 95%).
3
Q
What is the primary role of small leucine-rich proteoglycans (SLRPs) in tendons?
A
To regulate collagen fibril size and organization.
4
Q
What two SLRPs are dominant in tendon biology?
A
Decorin and fibromodulin.
5
Q
Which structural layer divides tendon fibers into visible fascicles?
A
Endotenon (or interfascicular matrix).
6
Q
Describe the “quarter stagger” pattern in collagen fibrils.
A
Tropocollagen molecules are displaced about one-quarter of their length from each other.
7
Q
What is the major non-collagen protein in young tendons?
A
Cartilage oligomeric matrix protein (COMP).
8
Q
In which tendon zone is collagen type II more prevalent, and why?
A
Fibrocartilaginous zone, to support compressive load.
9
Q
What effect does COMP have on collagen fibrils in vitro?
A
It accelerates collagen fibril formation.
10
Q
What are tenocytes, and why are they essential in tendons?
A
Cells responsible for the formation and maintenance of the extracellular matrix.
11
Q
Which type of tenocyte cells are most common in mature tendons?
A
Type I cells.
12
Q
What cellular structures allow tenocytes to communicate?
A
Long cytoplasmic processes linked by gap junctions.
13
Q
What roles do the endotenon and epitenon layers serve?
A
Endotenon carries blood vessels and nerves; epitenon surrounds the tendon.
14
Q
What structure surrounds tendons that are not within a sheath and helps reduce friction?
A
Paratenon.
15
Q
How does the paratenon contribute to tendon repair?
A
Supplies new blood vessels and cellular elements for repair.
16
Q
Why do tendons inside tendon sheaths heal more slowly?
A
Lack of the paratenon in the synovial environment limits repair.
17
Q
What structure allows smooth tendon movement over bony prominences?
A
Tendon sheath.
18
Q
What are the scuta, and where are they located?
A
Fibrocartilaginous pads on bony prominences, such as the distal limb.
19
Q
What is the function of the mesotenon within the tendon sheath?
A
Provides blood supply to the tendon.
20
Q
Which collagen type is primarily found in the mid-substance (tensional) region of tendons?
A
Collagen type I.
21
Q
What is the main difference between the cellular composition of tendons and ligaments?
A
Tendons have more type I tenocytes, while ligaments have varied proportions.
22
Q
Why might fibrocartilaginous zones in tendons have more type III tenocytes?
A
They are exposed to compressive forces.
23
Q
What characterizes type III tenocytes under light microscopy?
A
Round nuclei with visible nucleoli.
24
Q
What type of collagen is more common in regions subjected to compressive forces?
A
Collagen type II.
25
What is the purpose of biglycan and lumican in tendon regulation?
They modulate the function of decorin and fibromodulin in fibril formation.
26
How does the collagen organization vary along the length of a tendon?
It reflects the tendon’s biomechanical environment (tensional vs. compressive zones).
27
What percentage of tendon cellular elements are chondrocytes, synovial cells, and vascular cells?
5-10%.
28
What kind of collagen is present in smaller amounts in tendons besides type I?
Type III and minor collagens.
29
What process is involved in tendon growth after collagen fibrils form?
"Seed-and-feed" mechanism.
30
What are FACITs, and how do they function in tendons?
Fibril-associated collagens with interrupted triple helices; they affect fibril surface and packing
31
Which FACITs are thought to play a role during tendon development?
Collagens XII and XIV.
32
Which FACITs are thought to play a role during tendon development?
Collagens XII and XIV.
33
At what age do levels of COMP peak in equine digital flexor tendons?
Around 2 years of age.
34
What correlation exists between COMP levels and tendon strength?
Higher COMP levels are associated with greater tensile strength.
35
What findings have been observed in COMP-null mice?
No tendon abnormalities.
36
How does the mid-substance region of tendons differ from fibrocartilaginous regions?
It primarily contains collagen type I and small proteoglycans.
37
What are mesotenons composed of, and what is their role?
Layers of synovium; they often carry blood to the tendon.
38
What is the difference between endotenon and epitenon in tendons?
Endotenon carries blood vessels and nerves; epitenon surrounds the tendon. Endotenon surrounds fascicles within the tendon; epitenon surrounds the whole tendon.
39
Why is the paratenon less likely to rupture during tendon injury?
It can stretch considerably, absorbing strain.
40
What nuclear morphology characterizes
type I tenocytes?
Thin, spindle-shaped nuclei.
41
What function do synovial cells in the tendon sheath serve?
They produce synovial fluid for lubrication of the tendon within the sheath.
42
Figure 84-2. Cut surface of a frozen piece of SDFT revealing the extensive interfascicular tissue, the endotenon, which contains the internal vascular and nervous supply to the tendon and is responsible for interfascicular gliding movements (where most of the tendon’s stretch occurs). (Courtesy Smith RKW, Goodship AE. Tendon and ligament physiology.
43
Figure 84-1. Structural hierarchy of the tendon. The tendon is composed of increasingly smaller subunits, from fascicles visible to the naked eye (see Figure 84-2), to fibers seen under light microscopy, to individual collagen fibrils seen by electron microscopy. (I) Tendon unit surrounded by paratenon in extrasynovial locations and epitenon in synovial locations; II, third-degree fascicle (1- to 3-mm diameter); III, second-degree fascicle (400- to 1000-μm diameter); IV, first-degree fascicle (15- to 400-μm diameter); V, collagen fiber (1- to 20-μm diameter); VI, collagen fibril (20- to 150-nm diameter); VII, collagen triple helix (1-nm diameter); a, crimp.
44
Figure 84-4. The anatomy of a tendon within a tendon sheath. Note the absence of a paratenon and the presence of mesotenon attachments, which are incomplete along the length of a sheath and through which blood supply gains access to the tendon. I, Third metacarpal bone; II and III, proximal sesamoid bones; a, PAL; b, digital flexor tendon sheath wall; c, SDFT endotenon; d, mesotenon attachment; e, SDFT fascicle; f, DDFT; g, CDET.
45
Figure 84-5. Anatomy of the equine distal limb showing the important weight-bearing tendons and ligaments on the palmar aspect of the limb. It is these structures that most frequently suffer strain-induced injury. a, Accessory ligament of the SDFT; b, SDFT; c, accessory ligament of the DDFT; d, DDFT; e, SL; f, CDET; g, extensor branch of the suspensory ligament.
46
Figure 84-6. (A) The stress-strain curve for tendon showing its viscoelastic properties. The toe region is associated with elimination of “crimp,” and the linear region is where the tendon is operating in an elastic fashion. At the end of the linear region, the yield point is reached, where irreversible damage starts to occur before the tendon ruptures completely. (B) Hysteresis and conditioning. The loading and unloading curves are not the same, resulting in an energy loss, which is represented by the area between the two curves (hysteresis loop). If the tendon continues to be loaded repeatedly, the curve moves to the right until it reaches a steady state, when the tendon is more elastic. kN, Kilonewton. (Courtesy Smith RKW, Goodship AE. Tendon and ligament physiology.
47
Figure 84-7. SDF tendinopathy. Note the bowing, or swelling, of the palmar border of the right limb. Careful attention must also be given to the contralateral limb, which may exhibit a smaller swelling that can be easily missed (arrow).
48
What are the two primary processes for nutrient supply of tendons?
Perfusion and diffusion.
49
Where does diffusion primarily occur in tendons enclosed by a sheath?
Through the synovial fluid.
50
What are the three main blood supply sources for tendons?
Musculotendinous junction, osseous insertion, intra- and extratendinous vessels.
51
Which two vessels in the SDFT create an extensive vascular network around the tendon?
Longitudinally intratendinous vessels on the lateral and medial borders.
52
What results from ligation of intratendinous vessels in tendons?
Ischemic pathological damage.
53
Does removal of the paratenon blood supply cause damage to tendons?
No.
54
Which tendon has a lower blood flow in its fibrocartilaginous segment?
The deep digital flexor tendon (DDFT).
55
What vascular plexus supplies blood to the suspensory ligament (SL)?
Periligamentous vascular plexus.
56
How does age affect blood flow in tendons?
Blood flow declines gradually to the adult level by age 3.
57
What is the increase in blood flow during exercise in trained horses?
About 200%.
58
By how much does blood flow increase in an injured tendon?
More than 300%.
59
What are the two main functional types of tendons in horses?
Positional tendons and weight-bearing tendons.
60
What is the primary function of positional tendons?
To flex, extend, or rotate joints.
61
Why are weight-bearing tendons more elastic than positional tendons?
To store elastic energy for efficient locomotion.
62
Which joint helps optimize energy storage in the horse's distal limb?
The metacarpophalangeal (MCP) joint.
63
What is the role of the superficial digital flexor muscle in the horse's limb?
To fix the origin of the SDFT and dampen high-frequency oscillations.
64
At birth, how do the compositions of different tendons compare?
They are similar.
65
What environmental factor is believed to influence tendon differentiation postnatally?
Mechanical loading.
66
Which two tendons have similar matrix compositions in the equine distal limb?
SDFT and SL.
67
What structural component do weight-bearing tendons have more of compared to positional tendons?
High COMP levels and a mix of small and large collagen fibrils.
68
What happens to tendons where they change direction across the MCP joint?
They develop a cartilage-like matrix.
69
What type of crosslinks contribute to tendon biomechanical properties?
Covalent intra- and interfibril collagen crosslinks, and electrostatic crosslinks from noncollagenous proteins.
70
What waveform in relaxed tendon fascicles contributes to elasticity?
Crimp.
71
What is primarily responsible for tendon elongation under stress?
Sliding of fascicles over each other.
72
What type of sliding occurs in SDFT fascicles?
Rotational sliding.
73
What are the viscoelastic properties of tendons?
Tendon mechanical properties vary with the extent of stretch
74
What does the initial low-load stretch in the force-elongation curve of a tendon relate to?
Elimination of crimp in the fascicles.
75
What is determined from the linear portion of the force-elongation curve?
Stiffness.
76
What is the ultimate tensile strength of the equine SDFT?
Approximately 12 kilonewtons (kN) or 1.2 tons.
77
What can be plotted using tendon cross-sectional area and length?
Stress against strain.
78
What is the approximate ultimate tensile stress of the equine SDFT?
100 MPa.
79
At what percent of its length does the equine flexor tendon rupture?
At 10-12%, with reports up to 20%.
80
What strain percentages are recorded in the digital flexor tendons at different gaits?
3-8% at walk, 7-10% at trot, 12-16% at gallop.
81
What might the high strains in equine tendons indicate?
Their importance as elastic energy stores.
82
What does hysteresis represent in tendon mechanics?
The energy lost during the loading cycle.
83
What temperature can tendon cores reach during exercise?
Up to 44°C.
84
What is the effect of a rapid loading rate on tendon stiffness?
It increases tendon stiffness.
85
What effect does repeated loading have on tendon stiffness?
It decreases stiffness, known as conditioning.
86
How long does it take for tendons to recover after conditioning?
Significant resting time is necessary.
87
Why might the conditioning effect be less observed in horses compared to humans?
Horses are rarely recumbent for long periods, constantly loading their tendons.
88
What are the two main types of tendon injury?
Intrinsic (strain) and extrinsic (percutaneous) injuries.
89
What typically causes overstrain injuries in tendons?
Sudden overloading or progressive degeneration without repair.
90
Why might degeneration in tendons go unnoticed before injury?
Degeneration often lacks clinical signs of inflammation or repair response.
91
What findings in postmortem studies suggest prior tendon injury?
Asymptomatic lesions indicate healed, low-grade injuries.
92
What evidence supports the presence of tendon degeneration before injury?
Asymptomatic lesions, bilateral tendinopathy, age correlation, and exercise-induced degeneration.
93
How are bilateral tendinopathies significant in tendon injuries?
Often, one limb shows signs of degeneration that affect the contralateral tendon.
94
What association exists between tendon injury rates and age?
Increased injury rates correlate strongly with age.
95
What structural components increase tendon strength during development?
Size and number of collagen fibrils and crosslinks.
95
How does exercise affect tendon degeneration in adult horses?
Aging and exercise often lead to degeneration rather than adaptation.
96
How do crosslinks affect tendon strength?
They increase mechanical strength, with trivalent crosslinks being particularly important.
97
Why is the equine SDFT vulnerable to injury in adulthood?
Limited ability to adapt post-maturity and high strain in the central region.
98
What age is the SDFT mature in horses?
Around two years old.
99
What does matrix gene expression in mature tendons indicate?
Reduced expression in tensile areas after skeletal maturity.
100
How do glycosaminoglycan (GAG) levels change with age?
GAGs are reduced in tendons of long-term exercised and older horses.
101
What structural change occurs in tendon crimp angle with age?
Reduction of crimp angle in the central tendon core.
102
Why are core lesions common in tendon injuries?
Central fibers experience the most strain and rupture first.
103
How might genetics influence tendon injury risk?
Genetic variations in matrix proteins like tenascin-C are associated with injury risk.
104
What might cyclical loading cause in tendons?
Microdamage accumulation and potential degeneration.
105
Why may tenocytes fail to repair tendon damage?
Reduced cellular response, gap junctions, growth factors, and cellular senescence.
106
What response do aged tenocytes show to mechanical load?
They show a reduced anabolic response compared to younger tenocytes.
107
What role do matrix metalloproteinases (MMPs) play in tendon injury?
MMPs contribute to matrix degradation in response to injury.
108
Which MMP is elevated in both acute and chronic tendon injuries?
MMP13.
109
Which MMP shows reduced expression in tendon injury?
MMP3.
110
What role do ADAMTS proteins play in tendons?
They are implicated in cartilage and tendon degradation but show varying changes in injury.
111
What might unloading of damaged fibrils lead to?
Increased matrix degradation and apoptosis.
112
How does hysteresis affect tendons under load?
Causes heat buildup that may damage tendon proteins and cells.
113
What is the effect of core temperature during galloping on tendon cells?
High temperatures increase cytokine and enzyme production, potentially damaging tendons.
114
What adaptation do equine tenocytes have regarding high temperatures?
Greater resistance to heat than other fibroblasts.
115
How might hyperthermia contribute to tendon degeneration?
Increases matrix-degrading enzymes, weakening tendon structure.
116
Why might low oxygen levels affect tendon health?
Limited oxygen reduces synthetic and degradative activities of tenocytes.
117
What influences tendon degeneration during high-speed exercise?
High loading rates and repetitive mechanical stress.
118
What enzyme is commonly expressed in tenocytes under cyclic load?
Matrix metalloproteinase-1 (MMP1).
119
What cytokine is elevated in response to tendon stretching?
Interleukin-1β (IL-1β).
120
What age-related changes are seen in the collagen crimp angle of tendons?
It decreases, which affects the tendon’s mechanical properties.
121
How does age affect glycosaminoglycan levels in tendons?
GAGs are reduced in aging tendons, leading to degeneration.
122
What is a significant risk factor for tendon degeneration in horses?
Prolonged and repetitive high-speed exercise.
123
What is the first phase of tendinopathy?
Degeneration.
124
What triggers strain-induced tendon injuries in a “healthy” tendon?
Sudden overloading.
125
Which structure primarily supports the
MCP joint at heel strike?
The SDFT and SL.
126
When does clinical tendon injury occur?
When peak stresses exceed the tendon’s structural tolerance.
127
What is the primary function of the DDFT during locomotion?
Flexion of the distal interphalangeal joint during the swing phase.
128
What role does speed play in tendon injuries?
Increased speed raises the risk of tendinopathy due to higher loads.
129
Why might hard track surfaces increase tendinopathy risk?
They increase both speed and peak impact loading on the tendons.
130
How does fatigue impact the DDFT muscle?
It increases MCP joint extension, subjecting SDFT to higher strain.
131
How does heel elevation affect DDFT load?
It decreases DDFT load and may increase MCP joint extension.
132
What does toe elevation do to the MCP joint?
It decreases the degree of MCP joint extension.
133
What foot conformation is associated with increased tendon injury risk?
Low heel and long toe.
134
How do high pressures affect the DDFT near the MCP joint?
hey can cause “bursting” of the lateral or medial borders of the tendon.
134
What is a common site for tendon tears in synovial cavities?
The DDFT in the forelimb and the manica flexoria in the hind limb.T
135
How do tendon tears in synovial cavities often develop?
They may be exacerbated by synovial hypertrophy, PAL constriction, or adhesions.
136
What type of injury is a percutaneous tendon injury?
An extrinsic injury, usually due to trauma.
137
What is a consequence of severe trauma to the palmar metacarpal region?
Up to 50% tendon laceration can still allow full tendon function at walk.
138
What happens in the inflammatory phase of tendon repair?
emorrhage, leukocyte infiltration, and enzyme release.
139
What does the reparative (fibroblastic) phase entail?
Angiogenesis and fibroblast accumulation leading to scar tissue formation.
140
How does the collagen content in scar tissue compare to normal tendon?
Scar tissue has higher collagen III content than normal tendon
141
What property is increased in the healed tendon but compromises its efficiency?
Structural stiffness.
142
What cells are involved in tendon repair?
Resident tenocytes, endotenon and paratenon cells, and circulating cells.
143
How do intrinsic and extrinsic repair differ in tendon healing?
Intrinsic repair involves local cells; extrinsic involves cells from circulation.
144
What effect does TGF-β have after tendon injury?
It recruits fibroblasts and macrophages, promoting collagen expression.
145
What role does CTGF play in tendon repair?
It mediates fibrosis through TGF-β1 signaling.
146
What is the role of bFGF in tendon healing?
It promotes fibroblast chemotaxis, proliferation, and angiogenesis.
147
How does IGF-1 impact tendon repair?
It stimulates collagen synthesis and enhances healing stiffness.
148
What does VEGF do during tendon repair?
It promotes angiogenesis and tensile strength.
149
What family do BMPs and GDFs belong to?
The TGF-β superfamily.
150
What phenotype alteration occurs in BMP14 mutations?
Altered Achilles tendon phenotype.
151
How does EGF contribute to tendon healing?
It regulates cell growth, proliferation, and differentiation.
152
What response does PDGF-BB elicit in canine flexor tendon cells?
Increases cell proliferation and collagen production.
153
What is typically used to diagnose strain-induced tendon injury?
History, signs of inflammation, and lameness assessment.
154
How does inflammation relate to lameness in SDFT injuries?
Lameness corresponds more to inflammation than to damage severity.
155
What is the ideal timing for an initial ultrasonographic scan of an injured tendon?
Approximately one week after the injury.
156
What range of frequencies do modern ultrasound machines use for imaging tendons?
High frequencies between 7.5–15 MHz and above.
157
Why is it important to examine both limbs during ultrasonography?
One-third of strain-induced tendon injuries show bilateral ultrasound changes.
158
What are the characteristics of acute tendon pathology seen on ultrasound?
Enlargement, hypoechogenicity, reduced striated pattern, and shape or position changes.
159
How does chronic tendinopathy differ in appearance on ultrasound?
It shows variable enlargement, heterogeneous echogenicity, and fibrosis.
160
What marker indicates collagen I synthesis after tendon injury?
Carboxy-terminal propeptide of type I collagen (PICP).
161
Why might PICP levels rise after tendon injury?
Due to increased type I collagen formation in healing tissues.
162
What does COMP indicate in flexor tendon injuries?
It is elevated in synovial fluid in cases of tendon and ligament tears.
163
What role does serum COMP play in detecting tendon injuries?
It is less effective due to naturally high blood levels of COMP.
164
What is a common manifestation of SDFT injuries?
The formation of a core lesion seen on ultrasound.
165
Where is SDFT injury typically most severe?
Below the mid-metacarpal region.
166
How does desmopathy of the ALDDFT commonly present in ponies?
With mild or absent lameness and proximal metacarpal swelling.
167
What is a common cause of lameness in sports horses related to the SL?
Proximal suspensory desmopathy in the hind limb.
168
How can suspensory ligament branch injuries affect nearby structures?
They can tear into the MCP/MTP joint, causing effusion and lameness.
169
What complication can arise from collateral ligament injuries?
Secondary osteoarthritis due to joint instability.
170
What is the role of neoepitope markers in tendon disease?
They offer greater specificity in detecting tendon disease.
171
What is the indication of a superficial digital flexor tendon (SDFT) laceration in a loaded limb?
Hyperextension of the MCP/MTP joint (dropped).
172
How does a concurrent laceration of SDFT and DDFT affect the limb?
The toe is raised from the ground.
173
What happens when SDFT, DDFT, and SL are all transected?
Complete loss of MCP/MTP joint support; the joint contacts the ground.
174
Which tendons may be injured if the hind limb is caught in wire?
Cranialis tibialis, long digital extensor, or peroneus tertius tendons.
175
What symptom may result from digital extensor tendon lacerations?
Stumbling onto the dorsal MTP/MCP joint at a walk.
176
What were the traditional treatments described by Asheim in 1964?
Phlebotomy, cooling, plaster bandaging, and rest.
177
hat role does cold therapy play in tendon injury management?
Reduces inflammation, vasoconstriction, and analgesia.
178
Why is cold hydrotherapy preferred over ice packs?
Better contact and evaporation; lower risk of tissue damage
179
What duration of cold therapy is recommended?
No longer than 30 minutes to avoid reflex vasodilatation.
180
What advantage do equine spas offer in cold therapy?
Provide cold and compression, often with hypertonic saline.
181
What is the purpose of a Robert Jones bandage in acute injuries?
Reduces inflammation and edema by increasing interstitial pressure.
182
When should a palmar/plantar splint or cast be used?
For severe injuries with MCP joint hyperextension.
183
What shoe modification reduces tension on the DDFT?
Raising the heels.
184
How is increased palmar/plantar support achieved in shoeing?
By using a wider heel or egg bar shoe.
185
What shoe adaptation is recommended for SL desmopathy?
A shoe with an extended length or increased heel width.
185
How long might SDFT injuries require for rehabilitation?
Up to 12-18 months.
186
What indicates a reinjury in tendon rehabilitation?
Tendon CSA increase of more than 10% between exams.
187
What is ECSWT used to treat in horses?
Proximal SL desmopathy.
188
What is the hypothesized benefit of ECSWT on tissue?
Induction of analgesia and potential repair stimulus in chronic injuries.
189
What is the proposed benefit of therapeutic ultrasound?
Increases vascularization and fibroblastic proliferation.
190
How might low-level laser therapy aid tendon repair?
Stimulates cellular metabolism and collagen synthesis.
191
What is the clinical evidence for magnetic therapy in tendon healing?
None; effects remain anecdotal.
192
What are counter-irritation methods used in tendon treatment?
Chemical (blistering) and thermal cauterization (firing).
193
What effect does firing have on the treated tendon region?
Causes thinner, weaker skin without histologic benefits.
194
What are the suggested reasons for any benefit from firing?
Enforced rest, cytokine release, or protective tissue formation.
195
Which systemic medications are commonly used in acute inflammation?
Corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs).
196
Why should corticosteroids be avoided beyond the first 48 hours?
They inhibit fibroplasia, hindering tendon repair.
197
What is a potential adverse effect of topical DMSO?
Weakening of normal tendon tissue.
198
How do PSGAGs aid in tendon injury treatment?
Inhibit collagenase and macrophage activation, reducing inflammation.
199
When should intralesional injections be avoided after injury?
Within the first 3 days, to prevent hemorrhage increase.
200
What three components are typically involved in tissue engineering?
Scaffold, anabolic stimulus (e.g., growth factors), and cell source.
201
What role does IGF-1 play in tendon healing?
IGF-1 stimulates extracellular tendon matrix synthesis and acts as a mitogen.
202
What effect did IGF-1 injections have on initial swelling in tendinopathy models?
They decreased initial swelling compared to controls
203
Did IGF-1 show long-term effectiveness in tendon healing in natural disease studies?
No, it showed no significant long-term benefit over other treatments.
204
What negative impact did recombinant equine growth hormone (rEGH) have on healing tendons?
It reduced the yield point and ultimate tensile strength.
205
What is the main benefit of Platelet-Rich Plasma (PRP) in tendon repair?
PRP stimulates cell proliferation and matrix synthesis.
206
What does autologous conditioned plasma (ACP) contain compared to PRP?
Lower platelet concentration.
207
What specific proteins did PRP increase in equine tendon explants?
COL1A, COL3A, and COMP.
208
Is large-scale, high-quality clinical evidence available for PRP’s effectiveness in tendons?
No, large-scale trials of high methodological quality are lacking.
209
What was the initial purpose of autologous conditioned serum (ACS) in veterinary medicine?
To treat equine osteoarthritis.
209
What is the PAW classification in PRP treatment?
It considers Platelet numbers, Activation method, and presence/absence of White blood cells.
210
What anti-inflammatory mediator does ACS increase?
Interleukin-1 receptor antagonist (IL-1Ra).
211
What substance is used in ACS conditioning?
Chromium sulfate-coated medical-grade glass beads.
212
What material is ACell Vet made from?
Porcine urinary bladder submucosa.
213
What type of cells does ACell Vet aim to attract to injured tendons?
Mesenchymal stem cells (MSCs).
214
What are two essential characteristics of stem cells?
Ability to self-renew and differentiate into specialized cell types.
215
What is a risk associated with embryonic stem cells (ESCs) in horses?
Teratoma formation.
216
What is the difference between MSCs and ESCs in terms of differentiation?
MSCs are multipotent, whereas ESCs are pluripotent.
217
What is the typical dosage of MSCs used for treating SDFT lesions?
~50 million for minimally manipulated cells and ~20 million for cultured cells.
218
What is the main limitation in MSC differentiation into tendon fibroblasts?
Lack of a specific tenocyte marker.
219
Which growth factors are involved in MSC differentiation into tenocytes?
FGFs and GDF-5, -6, and -7.
220
What are the three hypothesized mechanisms of stem cells in tissue regeneration?
Secretion of regenerative factors, differentiation into tenocytes, and immunomodulation.
221
What are the two routes of MSC administration explored in the study?
Intraarterial and intravenous regional limb perfusion (RLP).
222
Which administration route had higher
MSC retention in the distal limb?
Intraarterial RLP.
223
Why was tendon splitting initially recommended for chronic tendinopathy?
To improve blood flow in damaged tendon tissue.
224
What issues led to tendon splitting’s decline in popularity?
Extensive granulation tissue, increased trauma, and persistent lameness
225
When is tendon splitting still advocated today?
For acute cases with a core lesion indicating a seroma or hematoma.
226
What surgical procedure aims to reduce strain on the SDFT?
Desmotomy of the accessory ligament of the SDFT.
227
What unintended effect can DALSDFT have on the SDFT?
It may increase strain due to MCP joint extension.
228
What newer instruments are used in desmotomy for improved visualization?
Loop-headed or hook-headed monopolar electrodes and bipolar radiofrequency probes.
229
