Ch 89-90 + F Ch 18

Developmental Orthopedic Disease (DOD)

Encompasses virtually all noninfectious orthopedic deranged developments of growing young horses Osteochondrosis is the most common Also includes cervical vertebral stenoic myopathy (Wobbler disease), collapse of cuboidal bones, angular and flexural limb deformities, subchondral bone cysts, and physitis

Osteochondrosis (OC)

Disorder itself

Osteochondritis

Inflammatory response to the disorder

Osteochondritis Dissecans (OCD)

An area of cartilaginous or osteochondral separation is present

OC latens

Focal osteonecrosis of the resting zone of the growth cartilage with adjacent vascular necrosis

OC manifesta

A later stage that includes focally impaired osteochondral ossification and cartilage retention

OC Dissecans

Characterized by cleft formation through the necrotic cartilage

Juvenile Osteochondral Conditions (JOCC)

Developmental orthopedic disorders that are related to the immature joint or growth plate Includes OCD, cuboidal bone disease, and various other forms of failure of the immature skeleton, but not cervical vertebral stenotic myopathy, flexural limb deformities, or angular limb deformities

Endochondral Ossification

In all mammals, the primordial skeleton is laid down first as a cartilaginous structures that starts to transform into bone during the fetal stage, a process that continues until well after birth

Fetal cartilaginous structures are well vascularized by vessels running through so-called cartilage channels

Ossification of the primary centers of ossification in the diaphyses of the long bones starts early in fetal life, and at the time of birth, all diaphyses are bony structures

Many secondary centers of ossification located in the epiphyses of the long bones and in other sites such as apophyses and cuboidal bones, are still partly cartilaginous at the time of birth

Longitudinal Growth of Long Bones

Longitudinal growth of long bones occurs at the growth plates or physes Chondrocytes originating from a germinal layer of cells (resting cells) undergo mitosis, proliferate, and subsequently hypertrophy and undergo apoptosis The chondrocytes are encased by a scaffold of extracellular matrix which forms the basis for the apposition of primary bone by osteoblasts that originate from the metaphysis The primary spongiosa that is formed will undergo continuous remodeling under the influence of biomechanical loading according to Wolff's law during the entire growth period of the foal Process of cartilage remodeling, followed by calcification of cartilage, deposition of primary bone, and successive remodeling into bony trabeculae as occurs in the young, growing animal, is known as endochondral ossification

Growth Process in the Epiphysis of Long Bones

In the epiphyses of the long bones, a similar growth process takes place, but is less advanced than in the diaphyses at birth Initially, there is a complete ring of cartilage around the ossification center that is located in the center of the epiphysis, connecting the cartilage at the articular side with the growth plate Ossification of this cartilage ring takes place first at the border of the physis and at the perimeter of the epiphysis The thick cartilage mass at the articular side of the epiphysis functions as a type of growth plate with simultaneously occurring processes of growth, remodeling, and ossification It is at this level that the characteristic lesions of equine OC develop After cessation of growth, a considerably thinner layer of articular cartilage remains in the mature animal Although macroscopically very similar, this layer is right from the start distinct from the growth cartilage

Joints Most Frequently Affected by OC

OC is most common in tarsocrural, femoropatellar, and metacarpo/metatarsophalangeal joints, but has been described in most other diarthrodial joints as well

Breed Differences in the Prevalence of OC Lesion Locations

In Warmbloods and Standardbreds, tarsocrural OC is most frequent, whereas in racing Thoroughbreds femoropatellar OC is predominant

Unillateral vs Bilateral OC Lesions

Most lesions present unilaterally, but are often found to be bilateral in the tarsocrural and femoropatellar joints and bilateral or even quadrilateral in the MCP/MTP joints

Concomitant Occurrence of OC Lesions in Other Joints

Concomitant occurrence in other joints or joint pairs is much less common, possibly because of the differences in time windows during which OC lesions develop in different joints

OC Predilection Sites in the Tarsocrural Joint

Cranial end of the distal intermediate ridge of the tibia

Distal end of the lateral trochlea of the talus

Medial malleolus of the distal tibia

OC Predilection Sites in the Femoropatellar Joint

Lateral trochlear ridge of the femur

OC Predilection Sites in the Shoulder Joint

Glenoid and the humeral head

OC Predilection Sites in the MCP/MTP Joints

Dorsal aspect of the sagittal ridge of MCIII and MTIII

Difference in OC Joint Fluid vs Traumatic Joint Fluid

OC joint fluid has in increase of the collagen degradation marker C2C while traumatic joint injury fluid has an increase in the collagen synthesis marker CPII

Timeline of Appearance and Regression of OC Lesions in the Tarsocrural Joint

Lesions originating during the first few months of life had mostly resolved at 5 months of age

Remaining lesions did not resolve

Timeline of Appearance and Regression of OC Lesions in the Femorpatellar Joint

Lesions originated from approximately 3 months onward, peaked at 6 months, and reached a stable condition around 8 months of age with most lesions healed

What is the age at which no further OC lesions will form nor will existing large lesions resolve?

At 12 months, for all joints, no major OC lesions should be formed, nor will existing large lesions be expected to resolve Resolution of minor lesions has been reported up to 24 months of age

Cartilage Turnover in Mature vs Young Growing Horses

Collagen turnover in mature cartilage is known to be virtually nil, but in young growing individuals, continuous remodeling and formation of cartilage takes place Huge difference in metabolism is reflected by the presence of synovial fluid levels of certain proteinases MMP-3, stromelysin levels are increased 80-fold in fetal joints compared to joints from mature individuals At 5-11 months of age, MMP-3 levels decrease dramatically, but are still two-to threefold higher than in mature joints

What are the two processes that clinical OC can be considered as the final outcome of?

The initiation of lesions by specific etiologic factors

Ensuing repair process

Flow Chart of Events Over time in Osteochondrosis

Vascular Events in Early OC: the Early Pathogenetic Mechanism

The thick layer of epiphyseal cartilage of the growing joint that is destined to change into bone via the process of endochondral ossification is nourished by vessels running through so-called cartilage canals

With ongoing ossification, these canals are obliterated in a process called chondrification, the timing of which is joint dependent Patent cartilage canals are not seen in proximal phalanx after 3 weeks of age, whereas they are still present at 4.5 months in the femoral condyle (but disappear by 7 months of age) The timing of canal abolishment in distal tibias was in between

The early pathogenetic mechanism of OC was the formation of chondronecrotic areas, caused by damage to cartilage canals, especially to the anastomosing branches that run through the ossification front from the bone marrow These initial chondronecrotic areas were clinically silent, not visible macroscopically or with the help of standard imaging methods and were called OC latens

Depending on environmental factors and the efficacy of the repair processes, these lesions would resolve or become clinically apparent, in which case they are designated as OC manifesta

In a genome-wide association study in pigs, a single nucleotide polymorphism (SNP) in the gene encoding T-box transcription factor 5 (TBX5) (a transcription factor interacting with two genes involved in vascularization) was significantly associated with OC lesion scores

The advancing ossification front induces a change in the arterial supply of the cartilage canals Initially supplied by arteries from perichondral origin, the advancing ossification front engulfs the midportion of the vessels in the canal, necessitating a shift towards subchondral, rather than perichondral arterial sources This shift suggests that crossing the ossification front leaves the vessels more vulnerable to mechanical influences

The secondary repair process follows almost immediately after the formation of the lesion

In one study at the age of 13-15 days, two vessels supplying the epiphyseal growth cartilage of the lateral trochlear ridge of the femur were transected in 10 pony foals which resulted in ischemic chondronecrosis that was associated with a focal delay in endochondral ossification (OC) in foals examined 21 days or more after transection In one foal a pathological cartilage fracture (OCD) was observed 42 days after transection

Vascular pathogenetic mechanism of OC can explain a number of commonly observed features of the disease, such as the joint-specific windows in time (related to joint-specific patterns in the progress of the ossificiation front and subsequent vascular rearrangements) and the frequent bilateral occurrence

The complex vascular rearrangements during the process of endochondral ossification are common to all individuals and not specific for those developing osteochondrotic lesions and offer no explanation for the individual susceptibility for OC It has been suggested that bacterial infections at early age may produce direct damage to the vascular structures, of which a large proportion has been shown to be surrounded by an acellular wall consisting of collagen type I, permitting bacterial binding A variety of more indirectly acting molecular mechanisms related to dysfunction of chondrocytes, extracellular matrix components, and signaling pathways have been suggested to play a role as well

Molecular Events in OC: The Possible Underlying Pathways

Osteochondrotic fragments could not be discerned from surgically created osteochondrotic fragments, however, the OC tissue bed stained positive for chondroitin sulfate and collagen type II, and the fracture bed did not

A comprehensive approach using both proteomics and metabolomics showed involvement of proteins related to cell cycle, energy production, cell signaling and adhesion, as well as chondrocyte maturation, extracellular matrix, and mineral metabolism, the lateral processes signifying a role for the subchondral bone as well

The role of the chondrocyte in OC Failure to undergo hypertrophy has been suggested as a main cause for OC or "dyschondroplasia, however this hypothesis is unlikely Chondrocytes harvested from early osteochondrotic lesions have a higher metabolic rate, but cannot be further stimulated to a higher level than chondrocytes from normal cartilage When harvested from longer-existing lesions, their metabolic rate is lower than in normal cells and stimulation is not possible This phenomenon may indicate a reactive upscaling of metabolic activity in response to lesion formation, which, when repair is unsuccessful, may develop into exhaustion and loss of vitality of the chondrocytes

Matrix Components in Osteochondrosis

Distribution of collagen VI was different in OC lesions compared to normal tissue

Differences in posttranslational modifications of collagen type II have been demonstrated in samples from early lesions

There was strong TGF-B mRNA expression in chondrocyte clusters immediately surrounding an OC lesion

OC cartilage showed increased expression of collagen types I, II, III, and X, and of MMP-13, ADAMTS-4, and TIMP-1 and decreased expression of TIMP-2 and TIMP-3

Expression of MMP-16 or membrane-type matrix metalloproteinase-3 (MT3-MMP) is not significantly altered in osteochondrotic cartilage

A strong increase in cathepsin B activity in chrondrocyte clonal clusters in OC has been demonstrated

Pellet cultures produced from OC tissues contained significantly less GAGs and there was an increase in activity of gelatinases (MMP-2 and MMP-9) in osteochondrotic cartilage

IGF-1 was found to be upregulated in osteochondrotic tissue, but was judged to be most likely related to the repair response rather than being primary

Signaling Pathways in Osteochondrosis

Significantly decreased Wnt-11 and increased B-catenin, Wnt-5b, Dkk-1, Lrp6, Wif-1, Axin1, and SC-PEP gene expression could be shown in early OC cartilage canal chondrocytes compared to controls

A Wnt signaling inhibitor, sclerostin, was strongly upregulated in OC lesions

Wnt signaling is known to regulate mitochondrial physiology and insulin sensitivity and abnormal mitochondria have been observed in the deep zone of OC cartilage

Heritability

Heritability (h2) is a statistic that estimates how much variation in a phenotypic trait in a population is a result of genetic variation

Can vary between 0 and 1.0

The higher the value, the bigger the influence of selective breeding on that trait

Heritability of OC in the Tarsocrural Joint

In most breeds heritability is highest for the tarsocrural joint with an average value around 0.30 but covering a range from 0.04 (Coldbloods) to 0.52 (Standardbred trotters)

Heritability of OC in the MCPJ/MTPJ

Approximately 0.15

Heritability of OC in the Stifle

In the stifle these values are lower, not rising above 0.10 with values as low as 0.05 for OC and 0.02 for OCD in the Dutch Warmblood

Heritability and Selecting for/against OC

Heritability measures the proportion of the phenotypic variance that is the result of genetic factors In theory, the higher the heritability, the quicker progress to eliminate a defect can be made by selection In practice, selection against OC has been proven extremely difficult, and progress, if any, has been slow Explanations OC is heavily polygenic with different genes involved in different joints resulting in a different h2 per joint Indications that different manifestations of OC (fragmentation versus flattening) may represent different traits Dynamic nature of OC Some traits that are known to be implicated in OC (such as a high growth rate) are seen as desirable and actively selected for or that certain conformational traits are both related with good athletic performance and increased risk for OC

Molecular Genetics of OC

Linkage and association analyses and genome-wide association studies have identified regions of the genome associated with some phenotypic manifestation of OC on about 2/3 of the 33 chromosomes of the horse

There is little overlap between MCP/MTP OC and tarsal OC, suggesting a different genetic background

Many of the identified quantitative trait loci (QTL) are breed specific

Many loci positively associated with desired traits in breeding have a relation with OC too

A different approach using leukocytes as cell source for DNA instead of articular tissues, identified dysregulation of a number of pathways, among others Wnt, Ihh, and TGF-B signaling in OC affected animals

The gene mannosyl glycoprotein acetylglucosaminyltransferase (MGAT4A) was the only gene to be strongly upregulated in all age groups with OC This gene is implicated in the intracellular transport of glucose and it can be conjectured that expression of this gene may be triggered by high levels of glucose and triglycerides, as resulting from the intake of high-energy diets Transient hyperglycemia peaks may lead to long-lasting changes through epigenetic changes, including superoxide anion-mediated mitochondrial damage Abnormal mitochondria and endoplasmic reticulum have been observed in the deep zone of OC cartilage

Environmental factors contribute relatively more to the manifestation of OC than genetics

What are the two major environmental influences playing a role in equine OC?

Loading

- Mainly determined by the exercise regimen

- Roughness of the terrain and conformation also may be contributing factors

Nutritional factors

- Can affect growth rate but may also influence hormonal balances, especially with respect to glucose metabolism, or can affect the mineral and trace element status of animals

Environmental Factors Affecting OC - Loading

A triggering role for biomechanical forces fits very well with the early pathogenesis of vessels in cartilage canals passing through a time window of enhanced vulnerability Whether or not a lesion will develop will be determined by the character of the biomechanical insult (magnitude, direction or force, repetition) and the degree to which the resistance of the vessel is impaired

Biomechanical (over)loading of joints may be caused by a variety of factors Irregular access to pasture Keeping animals in very large plots "mixed housing" (stabling overnight and pasture access during the daytime as opposed to the same environment day and night) Rough and slippery grazing grounds

Environmental Factors Affecting OC - Nutrition - Energy Intake

Growth rate is associated with OC, but this is irrespective of whether the high growth rate is caused by high nutritional levels or linked to genetic factors

Not so much overall growth rate but growth at defined age intervals that becomes significant

A high growth rate based on nutritional level is almost invariably linked to excessive intake of carbohydrates, often in an easily digestible form, such as concentrates This nutrition leads to a strong postprandial hyperinsulinemia This hormonal response varies between horses and may explain some of the variation in OC susceptibility Horses with OC have been shown to have higher post-prandial glucose and insulin responses to feeding higher-grain ratios than did unaffected horses

Insulin and its derivatives IGF-1 and IGF-II have a direct effect on the process of endochondral ossification, acting as mitogens for chondrocytes and stimulating chondrocyte survival or suppressing apoptosis OC-affected foals have a significantly lower IGF-I activity than OC-negative foals

Insulin also stimulates a rapid removal of the thyroid hormones T3 and T4 from the circulation T3 and T4 are involved in the final stages of chondrocyte differentiation and in the invasion of growth cartilage by blood vessels prior to its conversion to bone The effect of carbohydrates on thyroid hormone levels can be demonstrated in weanlings, but not in yearlings

Nutrition-related hormonal imbalances play a role in the development of equine OC, probably in increasing vulnerability for early vascular damage, however it is highly unlikely that it is the sole etiologic factor, as OC lesions can also be found in horses eating normal diets without any abnormalities in their insulin metabolism

Many lesions provoked by the administration of high-carbohydrate diets were similar, but not identical to clinical OC lesions

Many experimentally induced lesions were seen in the growth plate, where clinical OC is rarely, if even seen in horses

Environmental Factors Affecting OC - Nutrition - Imbalances of Minerals and Trace Elements

Imbalances in trace elements, in particular copper and its antagonists zinc and cadmium, have been implicated in the development of OC Mechanism was thought to act via lysyl oxidase, a copper-dependent enzyme that is essential for the formation of collagen cross-links Copper is no longer incriminated as being the main culprit for the development of OC

The calcium/phosphorous ratio is important for bone metabolism and (severe) aberrations will cause various bone disorders High calcium levels were shown to have no influence on the incidence of OC in foals, but high levels (four times the NRC recommendation) of phosphorous resulted in significantly more lesions Mechanism of action was suggested to be the induction of secondary hyperparathyroidism, which would lead to increased osteoporosis and subsequent weakening of the subchondral bone

Conservative Treatment of OCD

• Rest and controlled exercise

• Systemic NSAIDs and intraarticular medication may be administered but are not seen of great value

• Can only be successful in either very young animals in which there is still good capacity for regeneration, or in very mild cases

• Stifle lesions change over the longest period of time

When is healing of OCDs with conservative treatment deemed likely?

• Healing with conservative treatment is deemed likely when lesions are less than 2 cm long and less than 5 mm deep without radiographic fragmentation

When is conservative treatment advised with OCDs of MCIII/MTIII?

• When flattening without fragmentation (type IOC) occurs in the sagittal ridge of the MCIII or MTIII initial conservative treatment is advised

Conservative Treatment of OC in the Scapulohumeral Joint

• Conservative treatment of OC in the scapulohumeral joint was earlier seen as having a very poor prognosis, recent data suggests it may be a worthwhile option in mild cases where the glenoid cavity is involved

Prognosis for OCDs in the Femoropatellar Joint

• 64% success rate reported for the femoropatellar joint in a mixed population of racehorses and nonracehorses

  • Horses with smaller lesions (Grade I, <2 cm in length) were more successful than horses with larger lesions (Grade II, 2-4 cm and Grade III, >4 cm)

• 65% complete functional recovery in a more recent study in which depth of lesion was significantly associated with short-term complications (effusion and lameness), but not with the long-term outcome (UpRichard et al, 2013)

  • Involvement of structures other than the lateral trochlear ridge (patella, medial trochlear ridge) was associated with a worse prognosis

• In another study, 76% of arthroscopically treated horses were able to perform as intended (Vatistas, Wright, and Dyson, 1995)

Prognosis for OC Lesions in the Tarsus

• A recent study in a Standardbred trotters and pacers showed that when undergoing early removal of tarsal OC lesions, affected horses can be expected to perform equivalently to their unaffected counterparts (McCoy, Ralston, McCue, 2015)

• In a large survey of horses operated for tarsocrural OC, success rates were 73% in racehorses and 83% in nonracehorses (McIlwraith, Foerner, and Davis, 1991)

  • Synovial effusion resolved in 89% of racehorses and 74% of nonracehorses

• Score reductions for lameness and reaction to the flexion test of 80% to 90% and resolution of joint effusion in around 50% of cases of tarsocrural OC have been reported in a mixed population of Standardbreds and Warmbloods

Prognosis for OCDs of the MCP and MTP Joints

• In the MCP and MTP joints, a discrimination is made between lesions type I (flattening only), type II (flattening with fragmentation), and type III (flattening with or without fragmentation at the lesion site and a loose body present) of the sagittal ridge of MCIII/MTIII

  • Type I - treat conservatively

  • Type II and III - treat surgically shortly after diagnosing as treatment at a later stage is associated with the development of osteoarthritis

  • 90% return to athletic activity reported if the lesion is located in the more proximal part of the sagittal ridge, but lower rate for lesions in the weight-bearing area

Prognosis for OC of the Shoulder

• Shoulder OC has the least favorable prognosis

  • One study reports a favorable outcome of only 15% in racehorses (but better in nonracehorses) suffering from shoulder OC, which was similar after surgical or conservative treatment (Jenner et al, 2008)

  • Other reports mention successful outcome in approximately 50% of cases (McIlwraith, 2013)

Effects of OC on Performance

• For tarsocrural OC in Standardbreds, general trend is that fewer and smaller lesions may delay the start of the racing career but will have very little, if any, effect on performance

  • Severe or multiple abnormalities significantly compromise a potential future racing career

• Racing performance in Thoroughbreds treated for OC in the femoropatellar joint was not different from that in unaffected siblings, but fewer horses raced as 2 year olds and earnings were less, both at 2 and 3 years of age

• In a more recent study in racing Thoroughbreds (flat and hurdle racing), fewer horses with radiographic findings raced as 2 year olds and fewer were placed as 3 year olds compared to horses without radiographic anomalies (Verwilghen et al, 2013)

• In show jumpers, no differences between horses with tarsocrural OC and controls could be established, but OC of the femoropatellar and MCP/MTP joints significantly affected performance

Pathogenesis of SCLs

Originally SCL of the equine stifle were described as a manifestation of the osteochondrosis (OC) complex, resulting from retained, thickened, necrotic cartilage in the physis that infolds into the subchondral bone in the weight-bearing areas of the joint

Horses are usually of a young age

Another pathologic mechanism responsible for the development of SCLs is trauma to the articular cartilage, subchondral bone, or both Creates communication between the subchondral bone and the joint, allowing synovial fluid to gain access to the subchondral region under pressure and inducing necrosis of the adjacent bone which contributes to cyst formation

An articular fissure or fracture can lead to SCL formation In almost 1/3 of the cystic lesions, a concomitant fissure was visible on CT Most of the fissure lines had a midsagittal course and occurred in the proximal aspect of P1

Trauma can cause subchondral bone damage and bone ischemia and necrosis, followed by revascularization and resorption of necrotic bone, leaving a subchondral lesion

Bone trauma and secondary subchondral necrosis can also be the result of areas of contact of damaged articular cartilage affected by SCL

SCLs have been recognized after articular sepsis

Inflammation has been suggested as a contributing factor Analysis of the tissue lining and fluid found in SCLs in horses suggests that upregulation of inflammatory mediators may contribute to bone resorption and impaired healing of these lesions

Most Common Location of SCLs

Medial condyle of the femur

Percentage of SCLs in the Medial Femoral Condyle

45.8%

Percentage of SCLs in the Phalanges

26.2%

18.5% of all phalanges involved the distal sesamoid bone

Percentage of SCLs in the Carpal Bones

7.1%

Percentage of SCLs in the Third Metacarpal and Metatarsal Bones

6%

Macroscopic and Histologic Findings in SCLs

Show marked variation in size (from several millimeters up to >3 cm) and shape; may be shallow or deep (>10 mm) and may be dome-shaped, spherical, flattened, or without a particular shape

May be mild-to-intense sclerosis surrounding the cyst depending on the stage of development

Most lesions communicate with the articular cartilage

In histologic sections, most SCL are located within epiphyseal trabecular bone, rather than the subchondral bone plate

SCLs have a fibrous lining and may contain some fibrous tissue and/or gelatinous material Some lesions also contain fibrocartilage and necrotic bone

Cystic wall consists of elongated fibroblasts aligned parallel to collagen bundles, scattered macrophages, and polymorphonuclear cells

Hypervascularity and thickened bone trabeculae can be noticed in the adjacent bone

Cartilage overlying an SCL is generally normal looking except close to the canal, where signs of matrix degradation can be detected histologically on surgical explants

Clinical Symptoms of SCLs

• May or may not be associated with lameness

  • Lameness is attributed to pain from the joint (synovitis), the subchondral bone (increase in intraosseous pressure), or an increase in intracystic pressure, or a combination

  • In SCLs caused by osteochondrosis, lameness commonly develops at the start of training

  • In middle-aged to older horses, a traumatic event or correlation to ongoing intraarticular inflammation may be associated with onset of lameness

Diagnosis of SCLs - Radiography

• Typical radiographic finding is a dome-shaped or round-to-oval subchondral lucency with a variable surrounding sclerotic rim

• DP views best suited for detection of cystic lesions in the distal limb

• SCLs of the MFC usually diagnosed by a craniocaudal image but may be seen more readily in a caudolateral-craniomedial oblique or flexed lateral image

• Joint in the contralateral limb should also be evaluated because these lesions frequently occur bilaterally

• In a recent study, only 79% of SCLs diagnosed on CT were identified radiographically (Schon et al, 2017)

Diagnosis of SCLs - Computed Tomography

• CT is more accurate in the detection of small SCLs, their exact localization within the sagittal plane, as well as the detection of concomitant fissure lines

  • Fissure lines often associated with SCLs of the proximal P1, either mid-sagittal or parasagittal

• CT also allows detection of communication between the SCL and adjacent articular cartilage

  • In one study this was evident in 40/42 SCLs (Schon et al, 2017)

  • Commonly missed radiographically but appears to be a common characteristic of SCLs

• Recent study used CT to determine the morphologic characteristics of SCLs of the MFC (Walker et al, 2016)

  • In the sagittal plane all the lesions showed an articular communication in the cranial 15-20% of the MFC

  • Small and intermediate-volume SCLs were irregular and multilobulated, whereas large-volume SCLs had a more spherical appearance

Nonsurgical Treatment of SCLs

• Rest, NSAIDs, vitamin supplements, anabolic drugs

• Not successful, one study reported failure rate of 66% (von Rechenberg and McIlwraith, 1998)

• Other reports listed success rates of 45-64%

• In one study, no significant differences were found in racing results between yearlings with radiographically diagnosed SCLs in the MFC and unaffected horses, leading to the prediction that some lesions spontaneously resolve without treatment (Whitman et al, 2006)

• Limited exercise and intraarticular medication has a reported success rate of 64% with horses less than 3 years of age having a better prognosis for soundness

Benzyopyrone for Treatment of SCLs

• Benzyopyrone has been used systemically in horses with SCLs with 12/19 returning to normal use

  • Assuming pain associated with these lesions originates from increased intraosseous pressure, this drug should decrease the osmotic pressure in the bone that leads to lameness

Corticosteroid Injection for Treatment of SCLs

• Intraarticular injection of steroids (and hyaluronan) is often the first approach in the treatment of SCLs and leads to immediate improvement of the lameness, however risk of recurrence of clinical signs is very high

• Injecting corticosteroids into the lining of the SCL under arthroscopic or ultrasonographic guidance is based on work where inflammatory mediators were detected in the cystic contents leading to bone resorption

  • Corticosteroid is deposited throughout the cyst lining, with the most effective technique involving multiple redirections of the needle to distribute the medication

• In one study, lameness resolved in 67% of horses receiving injections and 77% were classified as successful based on follow-up lameness examination (Wallis et al, 2008)

Arthroscopic Approach for Surgical Treatment of SCLs

• Once the cyst has been identified, a rongeur can be used to remove the articular cartilage overlying the SCL

• Once all the cartilage not supported by underlying bone is removed, the contents of the cyst are evacuated with the help of a curette or motorized shaver

• Osteostixis of the adjacent bone is not recommended because it can lead to expansion of the cyst

• The contents and lining of the cyst are removed until the subchondral bone is visible

Transcortical Approach for Surgical Treatment of SCLs

• Most of the SCLs of the distal limb are not accessible through an articular approach and have to be debrided transcortically

• Should be performed under digital radiography, fluoroscopy, or CT guidance

• Skin incision over selected location advanced down to the bone

• Under fluoroscopic control, a 3.5 mm pilot hole is drilled through the bone into the cyst

• Once placement of the drill tip into the SCL has been verified, the drill hole is enlarged with a 5.5 mm drill bit to accept a small arthroscopic curette

Cancellous Bone Graft for SCLs

• Packing the lesion with autogenous grafts has been recommended but a study comparing healing of surgically created subchondral defects filled with compacted cancellous bone grafts with empty defects revealed no difference in the healing patterns after 6 months. This type of management is no longer used

Mosaic Arthroplasty for SCLs

• Autologous osteochondral grafting

• One study concluded that material properties of the grafts from the trochlear groove and axial aspect of the lateral trochlear ridge were the closest match for those found in the medial condyle, whereas properties of the lateral condyle were most similar to those found in the trochlear groove and axial aspect of the medial trochlear ridge of MCIII/MTIII (Changoor et al, 2006)

• In one study grafts of bovine, ovine, human, and equine origin were implanted in the femoral condyles of sheep (Waselau et al, 2005)

  • At 6 months equine grafts showed the best score for cartilage surface integrity and highest percentage for bone, thus having a better performance compared with grafts of other species

• Performed in a clinical case series of 11 patients where grafts were harvested from the abaxial border of the medial femoral trochlea of the unaffected limb (Bodo et al, 2004)

  • Grafts implanted through a small arthrotomy or by arthroscopy

  • All horses improved postoperatively, 10 had successful outcomes with radiographic evidence of successful graft incorporation and 7 returned to a previous or higher activity level

  • On follow-up arthroscopy there was successful reconstitution of a functional gliding surface with survival of transplanted hyaline cartilage

  • One horse had delayed incorporation of a graft because of a technical error but became sound

  • One horse had recurrence after 4 years of work and soundness

Tricalcium Phosphate Granules for SCLs

• Tricalcium Phosphate (TCP) granules used as filling material for SCLs of the distal limb following transosseous curettage

• When there is a large communication between the cystic lesion and the joint cavity, filling of the SCL with TCP granules is not recommended because of possible spread into the joint

• Before implantation, granules are placed in a syringe, autologous whole blood is added, and a vacuum is applied for several minutes to evacuate air from the granules

• Drill hole into the cyst and cyst cavity filled with the mixture

Parathyroid Hormone Application for Treatment of SCLs

• In humans when administered systemically and intermittently in low concentrations it has a strong anabolic effect on bone

• In a clinical case series of 15 horses that were lame because of an SCL at different anatomic locations, 11 became sound after debridement and filling of the lesions with PTH_1-34 in a fibrin hydrogel (Jackson et al, 2012)

  • Cysts curetted under arthroscopic supervision or through a transosseous approach followed by injection of the activated hydrogel

  • In arthroscopic cases, debridement of the cyst cavity was performed under fluid distension, fluid irrigation was then stopped and joint expansion was maintained by switching to CO2 and the cystic cavity was dried and blood and fluid removed

  • Gelation of the hydrogel took place within 1-3 minutes

  • When the transosseous approach was used the lesions were flushed after curettage and as much liquid as possible was removed through suction

Autologous Chondrocyte Implantation for SCLs

• Gold standard for repair of large cartilaginous lesions in humans

• A recent study demonstrated improved healing in the short (8 weeks) and long term (8 months) following implantation of autologous chondrocytes transduced ex vivo with a self complementary adeno-associated virus overexpressing IGF-1 in the equine femoral trochlea (Ortved at al, 2015)

Bone Morphogenetic Protein-2 for SCLs

• In one study the effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) in three horses suffering from five SCLs in the pastern joint was investigated (Jackson et al, 2017)

  • In all three horses, treatment resulted in increased bone density, decreased cyst size, and an absence of lameness

Screw Insertion for SCLs

• In a recent study, 20 horses with lameness attributable to an SCL in the MFC were treated with a transcondylar 4.5 mm cortex screw inserted in lag fashion without debridement of the lesions (Santschi et al, 2015)

  • By 120 days lameness was eliminated in 15 horses and the SCL area had decreased by 50% or more

• Good option for lesions in the distal limb

  • Often traumatic in origin and in almost 1/3 of the cases a concomitant fissure line is present when evaluated on CT

What are the two rationales for treating SCLs with bone screws?

• To improve bone remodeling in the cyst because of changes of the biomechanical environment in SCLs without concurrent fissure lines

• To stabilize fissure lines that can be a causative factor for the SCL

Miscellaneous Techniques for Treating SCLs

• Autologous patient-side grafting using bone marrow aspirate concentrate and PRP with TCP

• Injection of hydraulic biodegradable cement

• Titanium spongiosa balls of 5 mm used as filling material after debridement of SCLs

  • Surface microtopography of the implants has a major effect, influencing the interaction between the implant's surface and its biological environment, stimulating cell attachment, spreading, and proliferation of osteoblastic cells

  • Purpose is to enhance bone formation in the cystic cavity

  • In cases where arthroscopic supervision is used, after debridement of the SCL, the titanium balls can be inserted through a 5.5 mm drill guide and pushed into the bottom of the cyst cavity. Even in the presence of a large communication with the joint, the balls usually attach to the subchondral bone but to prevent migration into the joint a fibrin glue can be applied over the balls

Prognosis for SCLs

• Reports evaluating outcome in horses with SCLs of the MFC suggest that older horses, horses with preexisting OA, horses with bilateral lesions, and horses that have upright hindlimb conformation, such as Quarter Horses, have a significantly decreased prognosis for return to soundness following surgical intervention

• In one study of horses with MFC SCLs treated with arthroscopic debridement, 64% of young horses became sound while only 34% of mature horses (>3 years) returned to soundness

• Following surgical debridement of MFC SCLs, 64% of Thoroughbreds raced, compared with 77% of siblings

  • There was a difference in racing percentage based on the width of the surface defect: 60.6% of horses with surface debridement of 15 mm or less and 39.3% of horses with surface debridement of at least 15 mm started a race

  • Amount of cartilage surface involved seemed to be a better predictor of success than depth of the lesion

Polydactyly in Calves

• Front limbs generally affected

• Radiographs to determine the extent of abnormalities

Flexural and Hyperextension Deformities in Calves

• Congenital deformities are seen within 1 or 2 weeks of birth

• Other congenital abnormalities sometimes seen simultaneously with flexural deformity are cleft palate, dwarfism, and arthrogryposis

  • Lupine ingestion by the dam between 30 and 70 days of gestation may result in arthrogryposis

• Acquired flexural deformity is seen secondary to reduced weight bearing associated with a primary painful orthopedic disease

Clinical Presentation of Hyperextension Deformities in Calves

• Usually seen in newborn calves predominantly affecting the fetlock or carpus and tends to be bilateral unless a congenital malformation of a joint is involved

• Hypertension deformity is also seen associated with excessive long-term weight bearing and is often then unilateral

Management of Hyperextension Deformities in Calves

• Mild and moderate hyperextension is generally best managed by increased (yet still limited) exercise

  • If this is not successful at improving the condition within 1 week or the condition is severe, corrective shoeing is used

• Heel extension most successful corrective shoeing

  • If equine glue-on shoe used, both the cuffs of the shoe must be cut (usually dorsally) to prevent compression of the claws

• More severe deformity and deformity proximal to the fetlocks should be treated with splints and bandaging

• Prognosis usually favorable for all congenital hyperextension deformities without malformation to the bony structures

Clinical Presentation of Flexural Deformities in Calves

• Most commonly mild metacarpophalangeal or carpal flexural deformity

• Metatarsophalangeal joints involved rarely

• Acquired flexural deformity seen in older calves is generally unilateral and secondary to a severe orthopedic injury where the animal cannot bear any or only minimal weight on the affected limb

  • A dropped fetlock and varus deformity at the carpus of the contralateral limb is evidence of excessive weight bearing

Management of Flexural Deformities in Calves

• Mild cases of flexural deformity respond well when placed in housing with good footing

• Rather than spending extending periods standing, daily walking exercise is preferable

• Medical treatment indicated when no predisposing orthopedic anomaly is present and the limb can be manually extended so the toe's ventral aspect can touch the ground

  • Splint should be placed on the palmar aspect of the limb, starting at the heel (leaving the claws out) and extending to the proximal MCIII/MTIII (for MCP flexural deformity) or proximal radius (for carpal flexural deformity)

  • Cast can also be placed and removed/changed 2-3 weeks later

  • Oxytetracycline can be given to relax the muscles for more rapid correction but should be avoided whenever possible in calves due to nephrotoxicity

Surgical Correction of Flexural Deformities in Calves

• Indicated for calves not responding to splinting or with insufficient correction of the deformity to allow weight bearing

• Metacarpophalangeal flexural deformity is treated by sequentially transecting the SDFT, DDF, and suspensory ligament until the deformity is released

• Tendons of the flexor carpi ulnaris and ulnaris lateralis muscles are transected to treat carpal flexural deformity

Superficial Digital Flexor in Calves

• Superficial digital flexor muscle arises from the medial epicondyle of the humerus and divides in two parts, forming two distinct tendons: A deep tendon that passes through the carpal canal and a superficial tendon that passes outside the carpal canal. Both tendons fuse in the midcannon bone but divide at the fetlock into the medial and lateral digit, forming a sleeve that encircles the DDFT. Each divided superficial flexor tendon inserts on the proximal palmar aspect of their respective middle phalanx

Deep Digital Flexor in Calves

• DDFT passes into the carpal canal and lays dorsal to the SDFT until near the fetlock, where it divides to insert on the palmar aspect of the distal phalanges of the medial or lateral digit

Suspensory Ligament in Calves

• The suspensory ligament (interosseous muscle in young animals) originates from the proximal aspect of the metacarpal bone and divides at the midmetacarpal region, sending a band that joins the superficial flexor tendon. A few centimeters distally, the suspensory ligament divides into three branches

  • Two abaxial

    • Further divide distally into two branches that each attach to the corresponding medial and lateral sesamoid bone before continuing to their insertion on the palmar aspect of each proximal phalanx

    • Each suspensory ligament abaxial branch continues into an extensor branch that joins the abaxial aspect of the extensor tendons on the dorsal aspect of each digit

  • One middle

    • Passes through the intertrochlear notch and divides into two branches that each join the axial aspect of the extensor tendons of each digit

Surgical Treatment for Metacarpophalangeal Flexural Deformity in Calves

• 7.5 cm incision made over lateral (or medial aspect of the DDFT at the level of the midcannon bone

• Fascia surrounding the flexor tendon incised in the same plane

• SDFT and the connecting branches from the suspensory ligament are identified and elevated with curved hemostats

• SDFT and connecting branches from the suspensory ligament transected

• Extend the fetlock to assess the degree of correction

• If not sufficiently corrected, tendons of the deep digital flexor muscle are isolated and transected

• If deformity still not sufficiently corrected, the suspensory ligament is identified immediately caudal to MCIII, isolated with a curved hemostat, and transected

• When the superficial digital flexor tendons and their connecting branches from the suspensory ligament are transected, a splint is not needed postoperatively unless tension from the splint is needed to force additional extension for optimum correction

• If the deep digital flexor tendons are also transected, the limb(s) may need splint support up to 30 days

• If the deep and superficial flexor tendons plus the suspensory ligament are transected, destabilization of the palmar aspect of the carpus occurs

  • A splint that extends to the radius to give palmar support to the carpus needs to be placed on the back of the limb

Surgical Treatment of Carpal Flexural Deformity in Calves

• 10 cm incision starting at the accessory carpal bone and extending proximally made on lateral aspect of the carpus over the tendon of the ulnaris lateralis

• Incision extended bluntly until the tendons of the ulnaris lateralis and flexor carpi ulnaris tendon are identified, isolated with a curved hemostat, and transected

• Splint placed postoperatively on the palmar aspect of the knee unless full correction obtained

Angular and Rotational Limb Deformities in Calves

• Common to observe a calf with a valgus deformity and an external rotation

• A varus deformity is often associated with internal rotation

• Claws usually rotate outward with valgus and inward with varus except in cases of multiple angulations in a limb

Etiology of Angular and Rotational Limb Deformities in Calves

• Congenital angular deformity is very rare in cattle and reporedly is in the middiaphysis of the affected long bone when it occurs

• Congenital abnormalities most commonly involve multiple joints sometimes with flexural deformities

• Growth plate differential growth, commonly seen in horses, is rarely seen in farm animals unless associated with excessive weight bearing where varus deformity is seen

• Most calves have a mild carpal valgus deformity of approximately 7 degrees which is within the normal range for most farm animals and does not require treatment

• Intermittent pressure allows the growth plate to respond to the line of stress

• Partially through reduced blood flow, constant pressure reduces longitudinal growth from the affected physis plate

  • The uncompressed side of the physis maintains normal growth which results in an angular deformity (usually varus)

  • Often seen at the hock or carpus on the contralateral limb (limb without a painful orthopedic problem)

Clinical Presentation of Angular and Rotational Limb Deformities in Calves

• Although mild valgus deformity is relatively common, varus deformity is abnormal. If varus deformity is found unilaterally, the contralateral limb should be examined for a significant orthopedic injury as a cause for excessive weight bearing in the deformed limb/joint

• Obtaining radiographic evaluation is important in investigation of orthopedic injuries, which are often important causal factors in angular deformity in farm animals

Diagnosis of Angular and Rotational Limb Deformities in Calves

• DP view needed for examination of the anatomic location of the deformity and its measurement

Medical Management of Angular and Rotational Limb Deformities in Calves

• Trimming the claws of a young calf creates growth plate response to stress applied opposite the deformity so self correction occurs

• Trimming and other hoof manipulation is based on the principle that the hoof will turn in the direction of the longer claw or toward the side of the wider wall

• The lateral claw must not extend more than 1 cm, otherwise the stress on the lamina may cause inflammation and pain

• Acrylic or a shoe can also be applied to the claw to extend the lateral or medial claw

Surgical Management of Angular and Rotational Limb Deformities in Calves - Transphyseal Screws

• Transphyseal screws are placed across the growth plate to retard growth on the convexed side of the deformity

  • 1 cm stab incision made midway 2-3 cm above the growth plate (except for the hock where a stab incision is made at the most distal and extraarticular area of the appropriate malleolus)

  • Pilot hole drilled with a 2.5 or 3.2 mm drill bit

  • One self-tapping screw, 3.5 or 4.5 mm (usually 32-36 mm in length) is placed across the ipsilateral third of the growth plate

  • Implant removed as soon as the leg is acceptably straightened

Surgical Management of Angular and Rotational Limb Deformities in Calves - Closing Wedge Osteotomy

• Line is drawn parallel to the joint at the level of the pivot point

• Height of the second osteotomy site is calculated by using the angle of deviation at the pivot point

Surgical Management of Angular and Rotational Limb Deformities in Calves - Step-Wise Osteotomy

• Horizontal osteotomy line drawn parallel to the joint, starting at the pivot line but extending only through half the diameter of the affected bone in the dorsopalmar (plantar) plane)

• Line is drawn from the axial end of the horizontal osteotomy line and extends 5 cm proximally along the long axis of the bone

• Second vertical line the same length is drawn from the same starting point but angled to represent the previously measured pivot angle, the width of that wedge is measured

• The last osteotomy line is drawn horizontally from the proximal aspect of these two vertical lines and extending perpendicular to the long axis of the proximal bone

Surgical Management of Angular and Rotational Limb Deformities in Calves - Cylindrical (i.e. Dome) Osteotomy

• First the pivot point is identify and is referred to as the center of rotation of angulation (CORA)

• Angle of the deformity is determined from the intersection of the drawn line

• Dome or curve osteotomy is performed centered on the CORA

• This allows two curved bone ends to angulate and translate on each other to correct the deformity with maximal bone contact and the limb length is maintained because no bone is removed

Approach to Osteotomies in Calves

• Skin incision made over the dorso or dorsolateral aspect of the affected long bone

• Inverted V-shaped tenotomy of the common (or long) digital flexor tendon done exposing the diaphysis

• Incision extended to the affected bone and subperiosteal dissection exposes the bone before the osteotomies

• 2 mm Kirschner wire placed 2 cm proximal to the joint below and 2 cm distal to the joint above at 90 degrees to the long axis of the bone to be osteotomized to facilitate realignment of the bone ends after the osteomy

Surgical Techniques in Calves - Closing Wedge Osteotomy

• Using a reciprocating saw, affected bone transected parallel to the joint surface immediately distal to the level of the pivot point

• Height of second osteotomy is measured from the radiographs

• Starting on the convex side, the second osteotomy is extended to the opposite side of the bone until it meets the first osteotomy site

• Bone fragments fixed after wedge is removed

Surgical Techniques in Calves - Step-Wedge Ostectomy

• 3.2 mm hole drilled from dorsal to palmar (plantar) in the center of the bone at the intended start of the longitudinal osteotomy lines

• Second hole drilled 5 cm proximal

• Two holes prevent inadvertent longitudinal fissures associated with the creation of the longitudinal osteotomies

• Oscillating saw or Gigli wire used to join the two holes by a longitudinal osteotomy

• Using the width measurement of the wedge needed, another hole placed proximally and second longitudinal osteotomy is performed

• Horizontal osteotomies are made by cutting the bone parallel to the joint without extending any further than the distal aspect of the longitudinal osteotomies

• Proximal osteotomy site is done perpendicular to the long axis of the proximal fragment

• Distal osteotomy is made parallel to the distal joint

• Lag screws are applied across the vertical component created as part of the internal fixation repair

Surgical Techniques in Calves - Cylindrical or Dome Osteotomy

• Arc osteotomy using a biradial saw with the calculated arc of a circle centered on CORA

Prognosis for Angular and Rotational Limb Deformities in Calves

• Reasonable for angular deformities associated with growth plate imbalance, such as most valgus deformities

• Wedge osteotomies carry a fair prognosis for functionality, although a cosmetic defect due to enlargement at the surgery site is expected

• Prognosis for angular deformity secondary to contralateral orthopedic injury is generally poor because it is usually centered over a joint and is also dependent on the prognosis of the primary orthopedic injury