Equine Orthopedic Disorders Quiz

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Questions and Answers

Which type of tarsus is considered good for athletic performance?

Type III

Type II

Type I (correct)

Type IV

Angular limb deformity can only occur in the carpus.

False

What is the most common cause of angular limb deformity due to asynchronous growth?

Asynchronous metaphyseal growth

Medial deviation of a limb is referred to as __________.

Varus Signup and view all the answers

Match the following clinical signs with their descriptions:

Angular deviation = Limb deviation from the long axis in frontal plane Joint laxity = Excessive looseness of joint structure Cuboidal malformation = Deformity of cuboidal bones affecting limb alignment Physeal trauma = Injury at the growth plate of a bone Signup and view all the answers

Which of the following is NOT a common developmental orthopaedic disease in horses?

Hip dysplasia Signup and view all the answers

Incomplete ossification of cuboidal bones can occur in foals due to being born prematurely.

True Signup and view all the answers

What are the primary clinical signs of cuboidal bone hypoplasia?

Angular deviation of limb, excessive laxity, tarsal or carpal bone wedging/collapse Signup and view all the answers

Treatment for severe cases of cuboidal bone hypoplasia may involve using a _______ for 10-14 days.

tube cast Signup and view all the answers

Match the type of cuboidal bone compression with its description:

Type I = < 30% compression Type II = > 30% compression; fragmentation Signup and view all the answers

What is the primary ingredient in Cosequin?

Glucosamine HCl Signup and view all the answers

Cold application is not effective during the inflammatory phase of treatment.

False Signup and view all the answers

Name one method of physical therapy that helps to prevent capsular fibrosis.

Limb mobilization Signup and view all the answers

Acupuncture is considered a form of __________ therapy.

physical Signup and view all the answers

Match the following physical therapies with their uses:

Cold application = Reduces soft tissue perfusion Limb immobilization = Prevents further injury Swimming = Promotes limb mobilization Shockwave therapy = Provides short-term analgesia Signup and view all the answers

What is the most common area for osteochondritis dissecans (OCD) to occur?

Distal intermediate ridge of the tibia Signup and view all the answers

Subchondral bone cysts (SBC) always disrupt the articular surface.

False Signup and view all the answers

List one genetic factor that can predispose horses to osteochondritis dissecans (OCD).

Quantitative Trait Loci (QTL) Signup and view all the answers

In OCD, _____ is released during the inflammatory response, leading to pain.

cytokines Signup and view all the answers

Match the clinical signs with the related conditions:

Tarsocrural effusion = Osteochondritis Dissecans No lameness present = Subchondral Bone Cysts Joint pain = Osteochondritis Dissecans Fluid accumulation = Subchondral Bone Cysts Signup and view all the answers

Which of the following is NOT a proposed factor in the aetiopathogenesis of OCD/SBC?

Low energy diets Signup and view all the answers

Osteochondrosis can be diagnosed with radiography alone.

False Signup and view all the answers

What percentage of racehorses typically return to performance after early treatment for OCD?

75-80% Signup and view all the answers

Subchondral bone cysts may communicate with the _____ space.

joint Signup and view all the answers

Which imaging technique is deemed the treatment of choice for OCD?

Arthroscopy Signup and view all the answers

What percentage of draught horses typically has synovial effusion resolve over time?

60% Signup and view all the answers

All horses are equally prone to developing OCD, regardless of size or breed.

False Signup and view all the answers

Femoropatellar OCD primarily affects older horses.

False Signup and view all the answers

Name one condition that can induce subchondral bone cysts.

Trauma Signup and view all the answers

High phosphorus diets can be _____ times the National Research Council (NRC) recommendation.

5 Signup and view all the answers

What is the most common site for subchondral bone cysts in equines?

Medial femoral condyle Signup and view all the answers

Match the following locations to their frequency of occurrence in OCD:

Distal intermediate ridge of the tibia = Most common Lateral trochlear ridge of the talus = Less common Medial malleolus = Even less common Medial trochlear ridge of the talus = Least common Signup and view all the answers

The most consistent clinical sign of femoropatellar joint issues is ________.

distension Signup and view all the answers

What is the prognosis for a lesion that is less than 2 cm long?

78% success Signup and view all the answers

Concurrent lesions in multiple areas of the joint predict a better prognosis.

False Signup and view all the answers

Which horse breeds are most commonly affected by femorotibial OCD?

Thoroughbred, Quarter horses, Arabians, Warmbloods Signup and view all the answers

If there are radiographic lesions, some intervention is recommended, such as injecting a ________ into the joint.

corticosteroid Signup and view all the answers

What is the age range often seen for horses with subchondral bone cysts?

6 months to 15 years Signup and view all the answers

Match the type of intervention with its appropriate indication:

Conservative treatment = Mild cases with small defects Arthroscopy = Large lesions and if the horse is lame Medication with NSAIDs = Not very rewarding typically Corticosteroid injection = If there's radiographic lesions present Signup and view all the answers

How many femorotibial joints and femoropatellar joints generally communicate with each other?

About 70% Signup and view all the answers

The majority of horses presenting with SBC are typically older than 3 years.

False Signup and view all the answers

Which view is most rewarding for radiography in diagnosing SBC?

Flexed lateral view Signup and view all the answers

The primary clinical complaint from owners of horses with SBC is ________.

lameness Signup and view all the answers

What percentage of foals diagnosed with femoropatellar OCD may show an absence of ossification of the lateral trochlear ridge?

50% Signup and view all the answers

What is the success rate of a transcortical screw technique?

75% Signup and view all the answers

Osteoarthritis and traumatic joint disease are the most common equine health issues.

True Signup and view all the answers

Name one type of joint class based on anatomy.

Fibrous, cartilaginous, or synovial Signup and view all the answers

The fluid that nourishes and lubricates the joint is called __________.

synovial fluid Signup and view all the answers

Match the type of arthritis with its description:

Type I = Traumatic synovitis/capsulitis without major structural damage Type II = Trauma with damage to cartilage or major supporting structures Type III = Post-traumatic osteoarthritis with progressive deterioration Signup and view all the answers

Which of the following is NOT a manifestation of joint trauma?

Pulmonary inflammation Signup and view all the answers

Hyaluronan is a key component of articular cartilage, providing resistance to shear and tension.

False Signup and view all the answers

What is the typical cell count for normal synovial fluid?

5-19 x 10^9/L Signup and view all the answers

Type A synovial cells are primarily __________.

macrophagic Signup and view all the answers

Match the following substances with their function related to joint health:

PSGAG = Resists compression Collagen type II = Resists shear and tension Hyaluronan = Lubrication of joints Signup and view all the answers

What condition can develop after a trauma to a joint?

Osteoarthritis Signup and view all the answers

Meniscal tears are associated with traumatic arthritis.

True Signup and view all the answers

What are two common clinical signs of joint injury?

Swelling and pain. Signup and view all the answers

Chondroitin 4- & 6-sulfates are examples of __________ found in joint tissue.

glycosaminoglycans Signup and view all the answers

What is a common result of chronic stress-related subchondral bone damage in the fetlock joint?

Sclerosis and bone resorption Signup and view all the answers

Osteoarthritis typically causes progressive deterioration of articular cartilage and leads to improved joint function over time.

False Signup and view all the answers

List one type of IA fracture.

Slab fracture Signup and view all the answers

The most potent class of drugs used for osteoarthritis are __________.

corticosteroids Signup and view all the answers

Match the following treatments with their usage:

Hyaluronic acid = Modulates matrix synthesis/inflammation NSAIDs = Alleviate immediate effects of inflammation Pentosan polysulphate = Inhibits cartilage degradation DMOADs = Disease-modifying osteoarthritis drugs Signup and view all the answers

What is a primary clinical sign of osteoarthritis?

Joint stiffness Signup and view all the answers

Hyaline cartilage is easily regenerated after injury.

False Signup and view all the answers

What imaging method is used to evaluate cartilage and soft tissue?

MRI Signup and view all the answers

Commonly affected bones in IA fractures include the radial carpal bone and the __________ carpal bone.

third Signup and view all the answers

Which factor does NOT contribute to osteoarthritis?

Proper rehabilitation Signup and view all the answers

Capsulitis and synovitis can initiate the early stages of osteoarthritis.

True Signup and view all the answers

What is the goal of treatment for type III osteoarthritis?

To maintain quality of life Signup and view all the answers

Arthroscopy can be used to debride loose fragments and perform __________.

lavage Signup and view all the answers

Match the following diagnostic methods with what they reveal:

Radiography = Loss of joint space Arthroscopy = Anatomic evaluation Lameness exam = Localisation MRI = Soft tissue evaluation Signup and view all the answers

What is the ideal age for performing surgery on distal MCIII/MTIII deviations?

3 months Signup and view all the answers

The prognosis for mild/moderate cases of angular limb deformity is generally poor.

False Signup and view all the answers

What is epiphysitis?

Abnormal thickening of the physis/epiphysis. Signup and view all the answers

Surgical intervention is indicated for ___________ deviations.

moderate or marked Signup and view all the answers

Match the following surgical procedures with their descriptions:

Transphyseal bridging = Used for moderate to severe deviations Hemi-circumferential periosteal elevation = Stimulates growth on the slow-growing side Resection of physis = Applied in older weanlings Transphyseal hemi-circumferential periosteal elevation = Combined with foot trimming and confinement Signup and view all the answers

What dietary changes may help prevent epiphysitis in rapidly growing foals?

Reduce energy intake Signup and view all the answers

Flexural deformities are exclusively congenital and cannot be acquired.

False Signup and view all the answers

What is a primary clinical sign of epiphysitis?

Firm, warm enlargement of the physis. Signup and view all the answers

NSAIDs are used for __________ pain management in cases of skeletal deformity.

reducing Signup and view all the answers

Match the following clinical signs with the appropriate conditions:

Lameness = Common in flexural deformities Enlargement of physis = Indicative of epiphysitis Severe knuckling over = Associated with fetlock flexural deformity Palpation tenderness = Common in osteochondrosis Signup and view all the answers

What is a common treatment for mild flexural deformities?

Physical therapy Signup and view all the answers

Increasing nutritional intake is recommended for young horses with epiphysitis.

False Signup and view all the answers

What major risk is associated with severe angular limb deformities if not corrected early?

Osteoarthritis. Signup and view all the answers

A common result of osteochondrosis is the retention of __________ in the growth plates.

cartilage Signup and view all the answers

Match the following joint conditions with their associated age range:

Epiphysitis = 3-6+ months Distal radius issues = 8 months to 2 years Angular limb deformity = Birth to 6 months Flexural deformities = At or shortly after birth Signup and view all the answers

Study Notes

Developmental Orthopaedic Disease: Lameness in Young Horses

Common Developmental Orthopaedic Disease (DOD) in Horses:
- Cuboidal bone malformation
- Acquired angular limb deformity (ALD)
- Epiphysitis/physitis/physeal dysplasia
- Flexural limb deformities
- Osteochondrosis (OCD; SBC’s)
- Cervical vertebral malformation
- Juvenile arthritis

Cuboidal Bone Hypoplasia

Incomplete ossification of the cuboidal bones of the carpus or tarsus (or both)
Most cuboidal bone ossification occurs in the last 2-3 weeks of gestation, except in:
- Premature (< 320 days) or dysmature foals
- Congenital/developmental anomalies
Affected foals may also have decreased muscle tone and flexor tendon laxity.

Clinical Signs of Cuboidal Bone Hypoplasia

Angular deviation of limb (valgus, vertical?)
Excessive laxity – especially carpi & tarsi
Tarsal or carpal bone wedging and/or collapse (confirmed on radiographs)

Diagnosis of Cuboidal Bone Hypoplasia

Signalment & Physical Examination
Radiography (Wide joint spaces, small round cuboidal bones)

Grades of Cuboidal Bone Hypoplasia (Tarsus)

Type I: < 30% compression
Type II: > 30% compression; fragmentation

Treatment of Cuboidal Bone Hypoplasia

Minimize compressive forces and further injuries
Confinement (most important)
Severe cases: tube splints or tube casts for 10-14 days (difficult to manage in fast-growing foals)
Monitor ossification (re-radiograph at 2-weekly intervals)

Prognosis of Cuboidal Bone Hypoplasia

Carpus:
- Better with increasing grade (i.e. ossification)
- Carpal bone collapse = Poor
Tarsus:
- Type I: good for athletic performance
- Type II: poor for athletic performance

Angular Limb Deformity (ALD)

Limb deviation from the long axis in the frontal plane
Medial deviation = Varus
Lateral deviation = Valgus
May be accompanied by digital rotation
Occurs most commonly in the carpus, fetlock, and tarsus (other joints rarely)

Aetiology of ALD

Asynchronous metaphyseal growth is the most common cause
Other differentials: Joint laxity, Cuboidal malformation, Physeal trauma, Poor foot trimming, In-utero mal-positioning

Clinical Signs of ALD

Angular deviation (examine standing and at walk from different viewpoints)
Differential diagnosis = Joint laxity (Cuboidal bone malformation; windswept foals, ligament flaccidity)
Differential diagnosis = Joint swelling (Physeal trauma; fracture; sepsis)

Diagnosis of ALD

Physical findings:
- Visual presentation
- Identify the center of rotation
- Measure angles to assess the degree of abnormality (goniometry)
- Palpation findings: laxity, pain, etc.
- Trim & balance feet; re-examine on flat surface
Radiography:
- +/- Cuboidal bone abnormalities
- Identify center of rotation
- Goniometry on radiographs

Treatment of ALD

Age:
- Distal radial/tibial physes < 6 months (surgery 6 weeks - 12 months)
- Distal MCIII/MTIII < 3 months (surgery as soon as noticed)
Degree of deviation:
- Mild-moderate carpal deviation in foals < 4 months:
 - Small paddock/stall confinement
 - Trim feet (outside of feet for valgus)
 - Dorsomedial/dorsolateral feet extensions
- Frequent reassessment vital (Weekly)
- Especially for fetlock (short window of growth)  Surgery as soon as possible on fetlocks.

Surgical Procedures for ALD

Transphyseal hemi-circumferential periosteal elevation (stripping):
- Stimulates growth on the side of the growth plate that was growing too slowly
- Always with foot trimming & confinement
- Carpus by 4-5 months (up to 12)
- Fetlock by 2 months
Transphyseal bridging:
- For moderate to severe (> 15°) deviations
- Impairment of growth in the convex side of the limb
- Screws & wire or transphyseal screw (most common)
- 2-hole plate or staple
- Wedge or dome osteotomy for severe cases
Resection of physis (older weanlings):
- Carpus only
- Carpus by 4-5 months
- Fetlock by 3 months

Complications of ALD Surgery

Incision infection
Implant breakage
Excessive periosteal reaction

Prognosis of ALD

Mild/moderate cases are good
Fetlock varus more likely to result in fetlock/pastern OA
Severe ALD more likely to lead to OA if not corrected early
Generally perform at the same level as peers if treated

Epiphysitis/Physitis

Abnormal thickening of the physis/epiphysis
Multifactorial in origin (single/bilateral, multiple joints)

Aetiology of Epiphysitis/Physitis

Physeal injury/excess compression during active growing phase
Nutritional:
- Low dietary Cu & Zn
Limb overloading may lead to contralateral limb physitis

Signalment of Epiphysitis/Physitis

Foals +/- ALD
Fetlock: 3-6+ months
Rapidly growing wealing/yearlings – often large bodied for age:
- Distal radius: 8 months to 2 years
- Distal tibia: less commonly observed
- Overfed for rapid growth

Clinical Signs of Epiphysitis/Physitis

Firm, warm, enlargement of physis (most common on the medial side)
Usually occurs in the distal radius, tibia, MC/MT III
Usually painful on deep palpation
ALD/flexor tendon contracture
Lameness (can range from stiffness to reluctance to stand)
Distal radius or tibia; not usually both
- If distal MC/MT III; usually all 4 involved
Concurrent ALD or flexor tendon contracture in severe or chronic cases

Diagnosis of Epiphysitis/Physitis

Signalment & nutritional history
Physical examination findings:
- Palpation of all long bone physes
- Gait evaluation
Radiographs:
- Metaphyseal flaring
- Asymmetry:
  - Metaphysis
  - Cortical thickness
- Widening of the physis
- Wedging of the epiphysis
- Partial physeal closure/bridging

Treatment of Epiphysitis/Physitis

Reduce growth rate and/or body mass (only works on young, still growing horses)
Evaluate feed:
- Reduce energy intake
- Formulated diet
- Good quality grass hay; reduce/replace lucerne
- Reduce milk intake in nursing foals
- Early weaning
NSAID—Phenylbutazone 2-3 weeks @ lower doses
Stall confinement or minimize activity to prevent further physeal trauma (2 weeks to 2 months)
Corrective hoof trimming
Treat ALD or flexural deformities if present and young enough

Prognosis of Epiphysitis/Physitis

Mild cases are often self-limiting; may resolve with skeletal maturity
Good prognosis for athletic activity
Poorer for athletic career if conformation permanently affected
- Greater risk of injury; Severe carpal varus; Bench knee

Flexural Limb Deformities

Inability to extend limb fully due to difference between bone length vs soft tissues
Congenital flexural limb deformities:
- Apparent at or shortly after birth
- Reduction of functional length of the musculoskeletal unit
- Contracture of the SDFT & DDFT  Fetlock; carpus
- Contracture of the DDFT  Coffin joint
- Multiple structures usually affected
- Extensor tendon rupture

Clinical Signs of Flexural Limb Deformities

One or more limbs
Carpus (most common) or fetlock
Pastern, tarsus, coffin uncommon
Fetlock:
- Knuckle over at the fetlock
- Severe cases walk on the dorsal fetlock

Diagnosis of Flexural Limb Deformities

History: Problem at birth or during early growth
Physical examination:
- Unable to straighten limbs manually
- May have concurrent digital extensor tendon rupture (swelling over dorsal lateral carpus)

Treatment of Flexural Limb Deformities

Medical treatment (early or mild to moderately affected foals):
- Physical therapy: Extend limb for 10-15 minutes 4 to 6 times daily
- Oxytetracycline in the first 2 weeks: 2-4 g IV (44mg/kg)
- NSAIDs: Care with dose
Coaptation (bandages, PVC splints, compression boots, glue on toe extensions)
Surgery (usually last resort; superior check ligament desmotomy, inferior check ligament desmotomy, flexor tendon tenotomy)

Prognosis of Flexural Limb Deformities

Best prognosis for foals that can stand, ambulate, and nurse
- Respond in the first 2 weeks for athletic performance
Carpal contracture cases can take longer
Poor if unable to stand or there is deformity of the joints

Equine Osteochondrosis (OCD)

Failure of cellular differentiation in growing cartilage in metaphyseal growth plates and articular cartilage resulting in thickening or retention of cartilage
- i.e. failure of endochondral ossification

Osteochondritis Dissecans (OCD)

Disruption of the articular surface
Clinical signs due to inflammation:
- Degrading cartilage causes an inflammatory response  releases cytokines  Potentially causes nerve endings to sense pain  joint pain

Subchondral Bone Cysts (SBC)

Invagination of thickened plug of abnormal retained cartilage with various degrees of necrosis and inflammation
- +/- Disruption of the articular surface

Aetiopathogenesis of OCD/SBC

Heredity/Genetic predisposition
- E.g. 25-35% of variation in occurrence in the hock in SB horses
- E.g. Quantitative Trait Loci (QTL) associated with OCD in TB and Hanoverian WB
Nutrition:
- High energy diets – High soluble CHO content
- High phosphorus diets
- Copper deficiency
- Excessive zinc & cadmium
Biochemical trauma:
- Exercise is critical for normal bone and tendon development
- Conformation & increased body size may cause abnormal stress on joints and physes
- SBC induced following trauma (e.g. stifle)
Growth and Body size:
- Large, rapidly growing animals
- Most intense phase of growth occurs in the first 3 months
- Draught breeds – Prevalence is not higher [than other breeds]
- Not described in ponies

Clinical Presentation of OCD/SBC

Typical pattern:
- 1-2 lesions in characteristic locations (e.g. stifle, hock, fetlock)
- Often bilateral
Atypical pattern:
- Multiple articular + physeal lesions in characteristic and other random sites
- Guarded prognosis

Diagnosis of OCD/SBC

Clinical signs & radiographic signs  Pretty straightforward diagnosis if you have both
Clinical signs & no radiographic signs  Lesions seen only with arthroscopy or MRI/CT
No clinical signs but positive radiographic findings (“occult lesions”)
- Often seen in pre-purchase exams – Problematic as they have no clinical signs

General Clinical Signs of OCD/SBC

Young horse
Effusion
+/- Lameness:
- Inflammation due to synovitis
- Necrotic tissue debris
- Inflammatory cytokines
- Increased intra-osseous pressure

Osteochondrosis of Tarsocrural (Tibiotalar) Joint

Common areas of OCD:
- Distal intermediate ridge of the tibia (DIRT) - MOST COMMON
- Lateral trochlear ridge (LTR) of the talus
- Medial malleolus (MM)
- Medial trochlear ridge (MTR) of the talus

Signalment of Tarsocrural OCD

Usually weanling or yearlings; Young horses in training
Most common in Standardbreds
Less common in TB, quarter horses, Arabians, Warmbloods and draught horses

Clinical Signs of Tarsocrural OCD

Tarsocrural effusion (bog spavin)
Lameness uncommon
- If present, is more common in horses > 2 years old
“Occult” lesions may be seen on x-rays without clinical signs

Diagnosis of Tarsocrural OCD

Young horse plus effusion without lameness = Suspect
Radiography:
- Triangular osteochondral fragment off DIRT (most common)
- Irregularity of the lateral trochlear region +/- fragments
- Lesions frequently bilateral (~45-50% of Standardbred cases, ~70% of draught horse cases)
- X-rays may not accurately depict the amount of cartilage damage (ulceration)
- Lesions not observed on x-rays may be observed on arthroscopy

Treatment of Tarsocrural OCD

Arthroscopy:
- Treatment of choice
- Shorter convalescence
- Better function and a cosmetic result
- Mini arthrotomy for larger fragments
Arthrotomy:
- Less preferred treatment
- Longer convalescence
- Greater risk of complications
- Used for some very large DIRT fragments

Prognosis of Tarsocrural OCD

Racehorses:
- Good if you get to them early (75-80% return to performance)
- Poorer prognosis if there is articular cartilage erosion or degeneration
- Marked defects/degeneration in the trochlear ridges = bad
Non-racehorses:
- ~75% synovial effusion resolves
- May take 12-24 months for effusion to resolve
Draught horses:
- ~60% synovial effusion resolves
- Tend to have more marked synovial effusion

Osteochondrosis of Stifle/Femorotibial Joints

Femoropatellar joints:
- Lateral trochlear ridge of the femur (FLTR) - Most common femoropatellar OCD
- Medial trochlear ridge of the femur (FMTR)
- Patella: Usually concurrent with a trochlear lesion
Femorotibial joints:
- ~70% of the femorotibial joints and femoropatellar joints communicate with each other
- Subchondral bone cysts (more common)
  - Medial femoral condyle - Most common site of equine SBC’s
    - Highest load bearing part of the stifle (more than the lateral condyle)
  - Proximal tibia (sometimes)

Femorotibial OCD (Uncommon)

Signalment of Femorotibial OCD

Most cases presented at < 2yo
- ~56% diagnosed in less than 1yo, ~80% < 2 y old
Most common in TB, quarter horses, Arabians, warmbloods
May be diagnosed as early as 6 months of age with careful observation

Clinical Signs of Femorotibial OCD

Distension of the FEMOROPATELLAR JOINT (most consistent)
Lameness (none to severe depends on the severity of the lesion)
- Reduced cranial phase and foot arc
- ~60% bilaterally affected

Diagnosis of Femorotibial OCD

Signalment & clinical signs (young, effusion, no history of trauma)
Lameness examination (gait)
Radiography:
- Caudolateral to craniomedial view + Caudocranial oblique
- Irregular/flattened FLTR (lateral trochlear region)
- May be hard to see in foals
Ultrasound:
- Disruption of cartilage in LTR (dip in continuity)

Treatment for Femorotibial OCD

Conservative (mild cases):
- Restricted exercise & confinement
- Plus diet management
- Must be monitored – radiographs (may not be evident)
Arthroscopy (recommended)
- All cases with loose bodies and/or large radiographic lesions

Prognosis of Femorotibial OCD

Depends on lesion size, location:
- Lesion < 2 cm long: 78% success
- Lesion 2-4 cm long: 63% success
- Lesion > 4 cm long: 54% success
Concurrent FLTR, FMTR and/or patella lesions have a poorer prognosis
Multiple lesions in the joint = poor prognosis

Femorotibial SBC

Signalment of Femorotibial SBC

Most often occurring on the medial femoral condyle
Usually < 2yo on presentation; Most 1-3yo (range 6mo – 15yo)
Most common in Quarter horses &Arabians; Tend to see in TB in NZ
Owner’s usual complaint is lameness (most consistent initial finding)

Clinical Signs of Femorotibial SBC

Lameness: usually < grade 3/5
- Usually unilaterally lame even if lesions are present in both
- Few may be bilaterally lame
- Exacerbated by exercise +/- Loss of muscle mass
Swelling/effusion absent or minimal
Asymptomatic SBCs frequently occur

Diagnosis of Femorotibial SBC

Signalment & clinical signs
Lameness exam
Radiography:
- Flexed lateral view most rewarding
- X-ray both stifles – bilateral common
- Circumscribed area & sclerotic margin

Treatment of Femorotibial SBC

Consider: lesion size, 2° changes, age, lameness, cost, intended use
Conservative (not very rewarding in most horses)
- Rest & NSAIDS
- Medication of joint – Corticosteroids (e.g. betamethasone)
- Remodelling takes longer
- If no improvement after 3-4 months  Operate
Arthroscopy (recommended for large lesions and cases where the horse is lame)
- Debridement & lavage
- ± cancellous bone grafting for large cysts
Screw compression

Prognosis of Femorotibial SBC

Depends on the area of the joint surface affected, 2o changes, chronicity, etc.

Equine Joint Disease

Most common equine health issue.
Most common cause of lameness, impaired mobility, and loss of quality of life for humans, horses, and dogs.
Trauma-induced joint injury can be mild to catastrophic, ranging from acute synovitis to chronic OA.

Joint Anatomy & Biochemistry

Joints are classified into three anatomic classes: fibrous, cartilaginous, and synovial.
Joints can be simple or composite in complexity.
Joints can be high or low motion, including hinge and ball & socket types.
Synovial joints consist of subchondral bone, articular cartilage, synovial fluid, and a joint capsule.
- Subchondral bone: Provides support for joint structures.
- Articular cartilage: Specialized tissue that covers joint surfaces, resisting compression and shear forces.
  - Load-bearing cartilage: Found in weight-bearing areas.
  - Non-load-bearing cartilage: Found in areas with less force.
- Synovial fluid: Lubricates the joint and provides nutrients to the articular cartilage.
- Joint capsule: Encloses the joint and contains the synovium.
  - Synovium: Inner membrane responsible for producing synovial fluid and containing cells of mesenchymal origin.
    - Type A cells: Macrophages which are phagocytic.
    - Type B cells: Fibroblasts involved in secretion and synthesis of structural, anabolic, and catabolic molecules.
  - Fibrous layer: External layer of the joint capsule, providing strength and support.
  - Internal layer: Inner layer of the joint capsule, lining the joint cavity.
- Ligaments: Strong, fibrous bands that connect bones to bones and provide stability to the joint.
  - Intra-articular ligaments: Located within the joint capsule.
  - Peri-articular ligaments: Located outside the joint capsule.
Muscles and tendons play a role in joint movement and stability.
Articular cartilage is avascular (lacks blood supply) and aneural (lacks nerves), making it slow to heal and susceptible to degeneration.
- Resisting compression: Through its composition of polysulfated glycosaminoglycan (PSGAG) and hyaluronic acid (HA).
- Resisting shear and tension: Through its collagen type II structure.
- Doesn't regenerate: Making cartilage damage permanent and difficult to repair.
Synovial fluid biochemistry:
- Contains plasma ultrafiltrate with elevated HA.
- Minimal nucleated cells (less than 1x109/L).
  - Composed mainly of synoviocytes, lymphocytes, and monocytes (90%).
  - Small portion composed of neutrophils (less than 10%).
- Plays a role in joint nutrition and lubrication, through its HA content and GAG-associated water in cartilage.

Joint Response to Injury

Traumatic arthritis is OA that develops after trauma, either from a single event or repetitive episodes.
Other initiators of OA:
- Unmanaged clinical osteochondrosis.
- Post-recovery septic arthritis.
- Cuboidal bone hypoplasia.
Manifestations associated with joint trauma:
- Synovitis (inflammation of the synovial membrane and fluid).
- Capsulitis (inflammation of the fibrous joint capsule).
- Sprain (injury to joint ligaments).
- Subchondral bone microfracture and sclerosis.
- Intra-articular fractures (affecting articular cartilage and/or subchondral bone).
- Meniscal tears.

Classification of Traumatic Joint Injuries

Type I: Traumatic synovitis/capsulitis WITHOUT cartilage or major supporting structure damage.
- Examples: Acute synovitis, most sprains.
Type II: Trauma with damage to the articular cartilage or major supporting structures.
- Examples: Severe sprains, intra-articular fractures, meniscal tears.
Type III: Post-traumatic OA.
- Progressive deterioration of cartilage, bone, and soft tissues.

Trauma-Induced Joint Disease: Clinical Signs and Diagnosis

Clinical signs:
- Effusion (excessive synovial fluid).
- Swelling (soft tissue and bone).
- Pain (lameness and pain on flexion).
- Dysfunction (altered range and type of movement).
Diagnosis:
- Physical examination and lameness assessment.
- Imaging (radiography, ultrasound, CT, MRI).
- Scintigraphy and thermography.
- Synovial fluid analysis.
- Arthroscopy.

Synovitis & Capsulitis (Type I)

Etiology/pathogenesis:
- Acute vs. chronic.
- Preliminary event for OA development.
- Connective tissue degrading enzymes (e.g., metalloproteinases and proteinases).
- Cytokines and inflammatory mediators initiate and prolong cartilage damage.
Clinical signs:
- Primary synovitis (effusion without radiographic signs of bony change).
- Mild to moderate lameness (quick improvement).
- Differentiation between primary (synovial membrane), secondary (cartilage/bone/ligament), and infectious (bacteria, fungal, mycoplasma) synovitis is crucial.
Diagnosis:
- Synovial fluid analysis:
  - Total protein: Normal: 18 +/- 3 g/L.
    - Abnormal: > 25 g/L.
    - Severe inflammation: > 40 g/L.
  - Cell counts: Normal: 5-19 x 109/L.
    - Grey zone: 10-30 x 109/L.
    - Strong indication of infectious arthritis: > 30 x 109/L.

Villonodular Synovitis (Type I+)

Excessive synovial proliferative response.
Commonly found in the dorsoproximal fetlock and other regions.
Thickening palpable over the dorsal fetlock.
Diagnosed through radiographs and ultrasound.
Often unresponsive to intra-articular therapy.
Arthroscopic debridement is indicated.

Sprains & Dislocations

Injury of the supporting ligaments due to excessive forced movement.
Mild sprains (Type I):
- Minimal ligament fibers disrupted with potential hemorrhage.
- Capsulitis or synovitis (intra-articular ligament).
- Management: Rest, ice, support bandage, and NSAIDs.
Moderate sprains (Type I  II):
- Portion of the ligament torn with functional impairment.
- Variable severity of tears.
- Some heal by fibrosis.
- Management: Rest, ice, support bandage, and NSAIDs.
- Arthroscopic debridement if intra-articular.
Severe sprains (Type II):
- Partial/Complete disruption of the joint due to loss of ligament integrity.
- Damage to fibrous capsule, menisci, and tendons.
- Instability results in more severe pain.
- Management: Surgical reconstruction and splint/cast, arthrodesis (e.g., pastern joint).

Other Traumatic Injuries (Type II)

Tearing of intra-articular ligaments and meniscal tears.
Intra-articular fractures: Frequently accompanied by capsulitis/synovitis.
- Examples: Carpal "chip" fractures and slab fractures, proximodorsal P1 "chip" fractures, sesamoid fractures.

Intra-articular Fractures (Type II)

Carpus:
- Acute onset: Lameness, effusion, pain on palpation/flexion, and potential crepitus.
- Result of chronic stress-related subchondral bone damage: Sclerosis and bone resorption.
- Types: Osteochondral fragment, slab fracture, comminuted fracture.
- Common locations:
  - Radial carpal bone.
  - 3rd carpal bone.
  - Intermediate carpal bone.
  - Distal radius.
- Fragments can be free or attached to the joint capsule/bone.
Fetlock:
- Acute onset: Lameness, effusion, and potential crepitus.
- Result of chronic stress-related subchondral bone damage: Sclerosis and bone resorption.
- Types: Proximodorsal P1/P1, most common, distal MC3/MT4 less common, lateral & medial eminences of proximopalmar/proximoplantar P1.

Signalments, Diagnostics, Treatment, and Prognosis of Equine OA

Osteoarthritis (Type III)

Progressive and permanent deterioration of articular cartilage and other articular tissue.
End-stage result of:
- Severe trauma.
- Repetitive strain injury (wear and tear).
- Inadequately treated injuries/diseases (e.g., synovitis, sepsis, osteochondrosis).
Clinical signs:
- Lameness (pain).
- Early stages initiated by capsulitis/synovitis.
- Progressive joint dysfunction over time.
- Chronic swelling, joint stiffness, reduced range of motion.
- Palpable bony incongruence and loss of normal joint symmetry.
Diagnosis:
- Lameness examination: Localisation of the affected joint.
- Radiography:
  - Loss of joint space.
  - Osteophytes (articular bone spurs).
  - Sclerosis.
  - Enthesiophytes (mineralization of the joint capsule).
- MRI: Evaluation of cartilage and soft tissues.
- Arthroscopy: Anatomic evaluation and assessment of the severity of cartilage damage.

Treatment & Prevention of OA

Type I (Synovitis/Capsulitis):
- Objectives:
  - Alleviate immediate inflammation.
  - Prevent permanent fibrosis.
  - Treat and resolve the underlying cause if possible.
  - Minimize the development of OA.
- Management:
  - Early, timely, and appropriate pharmacologic intervention.
  - Ancillary therapy (e.g., cold therapy, limb support).
  - Minimizing instability.
  - Rehabilitation and maintenance of joint health.
- Control inflammation: NSAIDs, hyaluronan, corticosteroids, cold therapy.
- Protect cartilage: PSGAG, pentosan polysulphate.
- Support limbs: Padded bandages.
- Maintain mobility: Physical therapy to prevent fibrosis.
Type II (Articular Cartilage Damage):
- Objectives:
  - Repair/regenerate damaged cartilage.
  - Prevent further cartilage degeneration.
  - Minimize pain and improve function.
- Management:
  - Arthroscopy: Debridement of loose fragments and flaps, lavage, and treatment of partial-thickness defects.
  - Osteochondral grafts.
  - Stem cell therapy.
  - Post-operative care and rehabilitation.
  - DMOADs (e.g., Cartrophen).
Type II (Intra-articular Fractures):
- Objectives:
  - Stabilize the fractures.
  - Reduce inflammation.
  - Promote healing.
  - Restore joint function.
- Management:
  - Arthroscopy: Debridement of loose fragments/flaps, lavage, and reduction/fixation of larger fragments.
  - Post-operative support bandage and NSAIDs.
  - Stall rest (~2 weeks).
  - Rehabilitation plan: Hand walking, passive mobilization, swimming, or turnout (~8 weeks).
  - Slab fractures require ~6 months to heal.
  - Post-operative medication plan: Hyaluronan, PSGAG, corticosteroids (IA, IM, IV).
  - Prognosis: Determined by joint(s) injured, fracture configuration, injury severity, and cartilage loss.
**Type III (OA): **
- Objective: Maintain quality of life.
- Palliative relief: Minimize pain, discomfort, and dysfunction.
- Arthrodesis: Fusion of low-motion joints (e.g., pastern joint) to provide stability in infected or traumatized joints.
- Management:
  - Alleviate inflammation.
  - Prevent fibrosis.
  - Treat the underlying cause.
  - Early intervention.
  - Rehabilitation and maintenance of joint health.
- Pharmacologic intervention: NSAIDs (e.g., phenylbutazone, flunixin meglumine, meloxicam, ketoprofen), hyaluronic acid (IA or IV), PSGAGs (e.g., Cartrophen), pentosan polysulphate, IA corticosteroids (e.g., triamcinolone acetonide, betamethasone, methylprednisolone acetate, dexamethasone phosphate, isofluprednisolone).
- Biologics: Autologous conditioned serum, bone-derived mesenchymal stem cell therapy, fat-derived mesenchymal stem cell therapy, IRAP, platelet-derived therapy.
- Oral supplements: GAGs/HA/glucosamine (e.g., Flex-free, Syno-Flex, Cosequin).
- Physical therapy:
  - Cold application: Applied during the inflammatory phase (0-4°C for 30 minutes).
  - Limb immobilization: Prevent further injury and support unstable joints.
  - Limb mobilization: Prevent capsular fibrosis and maintain mobility.
  - Other therapies: Acupuncture, therapeutic ultrasound, soft tissue lasers, shockwave therapy.
- Prognosis:
  - High-motion joints: Poor long-term prognosis.
  - Low-motion joints: May tolerate OA for many years with treatment.

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Test your knowledge on equine orthopedic disorders, including angular limb deformities and cuboidal bone hypoplasia. This quiz covers conditions affecting athletic performance and their clinical signs, offering insights into common developmental orthopedic issues in horses.