Diagnosticul și tratamentul osteoartritei diseccans la cabaline

1. Introduction

The healing process of articular cartilage injuries is prolonged and requires significant effort from the body. This is primarily due to the lack of vascularization and the unique method of nutrient diffusion through imbibition, which makes articular cartilage one of the most challenging tissues in the body to regenerate.

Articular cartilage is a fundamental component of synovial joints, playing a crucial role in joint function. Its characteristics – including thickness, cellular density and matrix composition – vary not only between different joints, but also within the same type of joint among individuals.

All synovial joints contain articular cartilage composed of the same essential elements, serving a similar function. The unique properties that distinguish it include its exceptional resistance to compressive forces, its high durability against wear, and its ability to distribute mechanical loads both across the joint surface and over a larger area of the underlying subchondral bone. No synthetic material has yet been able to replicate these properties over a long period.

Extensive research has been conducted to better understand the factors leading to cartilage degradation and compositional changes, as well as the mechanisms involved in its repair and regeneration, aiming to restore its function.

Osteochondritis dissecans (OCD) is among the most significant orthopedic conditions affecting horses, regardless of breed. This disorder arises due to a disruption in the physiological process of endochondral ossification within the articular-epiphyseal cartilage complex (AECC) during growth. This alteration results in the formation of loose cartilage fragments within the joint, primarily due to the biomechanical impact of movement.

2. Histological and functional structure of articular cartilage

2.1. Functional and histological structure

Hyaline cartilage is a highly specialized, low-friction tissue with remarkable wear resistance, designed to withstand and evenly distribute mechanical loads. Despite its durability, it has limited regenerative capacity due to its low metabolic activity. It is composed primarily of chondrocytes embedded in a dense extracellular matrix rich in water, collagen, and proteoglycans. However, chondrocytes account for only about 5% of its total wet mass, and their metabolic activity is crucial for maintaining the balance between anabolic and catabolic processes, ensuring cartilage homeostasis.

The combination of fluid and matrix components gives articular cartilage its viscoelastic and mechanical properties, allowing it to efficiently distribute loads. Structurally, cartilage is stratified into four distinct layers: the superficial, middle, deep, and calcified cartilage zones (Figure 1).

The superficial (tangential) zone – which accounts for 10-20% of cartilage thickness – is the most collagen-rich layer, consisting of densely packed collagen fibers aligned parallel to the surface. It has the lowest compressive resistance, but deforms significantly more than the deeper layers. This zone also contains elongated chondrocytes that primarily produce lubricating and protective proteins, including superficial zone protein (SZP), which plays a critical role in maintaining joint lubrication.

The middle (transitional) zone makes up 40-60% of the cartilage volume. Its collagen fibers are thicker and arranged less uniformly, with an oblique orientation relative to the joint surface. The chondrocytes in this zone are rounder compared to those in the superficial layer.

The deep zone constitutes approximately 30% of the cartilage and contains the largest collagen fibers, which are aligned perpendicular to the joint surface. This layer has the highest concentration of proteoglycans and the lowest water content, providing it with the greatest resistance to compressive forces. The chondrocytes here are arranged in columnar structures, parallel to the collagen fibers, but perpendicular to the joint surface.

Beneath this layer, the calcified cartilage zone serves as a transition between cartilage and subchondral bone. It is characterized by small chondrocytes embedded in a calcified matrix, which helps anchor the cartilage to the underlying bone, ensuring structural stability.

2.2. Vascularization and nutrient exchange

Cartilage lacks direct vascularization and relies on diffusion from synovial fluid and subchondral bone for nutrient exchange. However, during early development, vascular channels in the AECC supply oxygen and nutrients. Disruptions in this process contribute to OCD development by causing focal ischemic necrosis of growing cartilage.

3. Pathophysiology of osteochondritis dissecans

3.1. Endochondral ossification and cartilage development in mammals

In mammals, the primordial skeleton initially consists of cartilaginous structures, which undergo simultaneous growth and transformation into bone throughout fetal development. Unlike mature articular cartilage, fetal cartilage is highly vascularized, with blood vessels passing through cartilage canals. The primary ossification centers in the diaphysis of long bones begin forming early in the fetal stage, ensuring that by birth, these structures are fully ossified. However, secondary ossification centers in the epiphyses, along with structures like apophyses and cuboidal bones in joints, remain partially cartilaginous at birth.

After birth, longitudinal bone growth occurs in the growth plates (metaphyses), where chondrocytes from germinal layers proliferate and form a structural framework of the extracellular matrix. These chondrocytes undergo hypertrophy, followed by apoptosis, allowing osteoblasts from the metaphysis to remodel the primary spongiosa. This spongy bone undergoes continuous remodeling, influenced by biomechanical loading throughout the foal’s growth, in accordance with Wolff’s Law.

This remodeling process continues in adulthood, adapting to changes in mechanical stress, such as those introduced by athletic activities. The sequence of cartilage remodeling, cartilage calcification, primary bone compaction, and subsequent transformation into trabecular bone is known as endochondral ossification. Simultaneously, long bones grow in diameter through periosteal development, leading to the formation of compact bone with Haversian canals.

Differences in ossification between epiphyseal and metaphyseal regions

Epiphyseal bone growth follows a similar pattern to that in the metaphysis, but with an incomplete ossification process at birth. This results in significant differences between joints during the ossification periods. In some joints, a complete cartilaginous ring surrounds the ossification center at birth, acting as a link between articular cartilage and the growth plate. Ossification of this cartilage ring begins at the metaphyseal margin and the epiphyseal contour.

The dense cartilaginous mass of the epiphyseal surface functions similarly to the growth plate, undergoing simultaneous growth, remodeling and ossification. Over time, this leads to a considerably thinner articular cartilage layer in adults. This precise location is where characteristic lesions of equine osteochondrosis develop.

Chondrocyte organization in growth and epiphyseal cartilage

Chondrocytes in both growth plate and epiphyseal cartilage are organized into four zones:

Resting zone – contains chondrocytes with low division rates, serving as precursors for proliferative cells.

Proliferative zone – rapidly dividing chondrocytes, which form well-defined columns in growth plate cartilage, while in epiphyseal cartilage, their arrangement is less structured and resembles clusters.

Hypertrophic zone – chondrocytes undergo differentiation, secreting a specialized matrix that facilitates cartilage calcification, acting as a scaffold for osteoblast-mediated bone formation.

Calcified zone – osteoclasts resorb the transverse septa, allowing vascular invasion and progenitor cell migration into the newly formed lacunae, where hypertrophic chondrocytes have disappeared.

The vascular endothelial growth factor (VEGF), produced by hypertrophic chondrocytes, is essential for vascular proliferation and cartilage vascularization (Gerber et al., 1999). The invasion of cartilage by blood vessels is crucial for endochondral ossification, as disruptions in angiogenesis due to genetic, biochemical, or mechanical factors lead to thickening of the growth plate due to hypertrophic zone expansion.

On the ossified surface, osteoblasts line the remaining longitudinal septa, forming histologically visible ossified cartilage spicules with an overlying bone network. The primary spongiosa, composed of calcified cartilage, bone trabeculae, and bone lamellae, undergoes osteoclastic remodeling, eventually replacing both calcified cartilage and the initial trabecular structure.

Regulation of chondrocyte proliferation and differentiation

Bone growth and chondrocyte differentiation occur in a three-dimensional process, influenced by genetic, nutritional, metabolic and mechanical factors. Mechanobiology has demonstrated that cartilage development and ossification accelerate under shear stress (weight-bearing activities) and slow under hydrostatic pressure (compressive loading).

Several studies have shown that growth plate chondrocyte proliferation is regulated by a local feedback loop dependent on spatial-temporal factors and involving three key signaling molecules produced by chondrocytes:

• parathyroid hormone-related peptide (PTHrP)
• Indian hedgehog (IHH)
• transforming growth factor-beta (TGF-β).

This feedback mechanism controls the transition of proliferative chondrocytes into terminally differentiated hypertrophic chondrocytes.

PTHrP – a peptide hormone similar to parathyroid hormone (PTH) – is synthesized and secreted by perichondral periarticular cells and chondrocytes at later developmental stages. It maintains continuous chondrocyte proliferation within the growth plate and prevents premature hypertrophic differentiation. This regulation ensures a stable pool of proliferative cells and prevents premature maturation into pre-hypertrophic and hypertrophic chondrocytes.

IHH – a cell-surface associated ligand – is secreted by prehypertrophic and hypertrophic chondrocytes to stimulate chondrocyte proliferation and sustain PTHrP activity at the ends of the developing bone. By inhibiting chondrocyte maturation, PTHrP negatively regulates IHH expression in cells at the terminal portion of the bone.

Additional molecular pathways in chondrocyte maturation

Runx2: a key transcription factor in chondrocytes, initiating hypertrophic differentiation and regulating chondrocyte maturation and proliferation by activating IGF and subsequently PTHrP.

TGF-β: secreted by perichondral cells in response to IHH, TGF-β enhances PTHrP synthesis, indirectly inhibiting hypertrophic chondrocyte differentiation. TGF-β can also directly suppress hypertrophy within chondrocytes.

While this feedback loop is considered the primary regulator of chondrocyte proliferation and bone growth, additional signaling molecules are likely involved in coordinating this network of regulatory factors.

3.2. Cartilage canals

Although the epiphyseal growth cartilage matrix appears similar to the overlying articular cartilage, it can be distinguished histologically or through perfusion studies due to the presence of blood vessels. These vessels, originating from the perichondral plexus, infiltrate the cartilage using the cartilage canals, whereas articular cartilage remains avascular. Cartilage canals are present in both growth cartilage and epiphyseal cartilage, and have been observed in mammals and birds – Figure 2. They typically extend from the epiphyseal region, forming a network of arterioles and capillaries, structurally resembling the glomerular capillary network of the kidney. These capillaries return to the perichondral plexus via venules, but anastomoses between cartilage canals have not been detected. However, cartilage canals may connect to the underlying bone, linking with marrow-derived vessels.

The exact function of cartilage canals remains unclear, but they are believed to serve three main purposes: nutrient supply to chondrocytes beyond the diffusion range of synovial fluid, formation and maintenance of secondary ossification centers, and delivery of mesenchymal stem cells to bone and cartilage.

As growth progresses, the ossification rate surpasses cartilage expansion, gradually thinning the growth cartilage layer. During this period, cartilage canals regress in a physiological process called chondrification, where blood vessels degenerate, and mesenchymal cells differentiate into proliferative chondrocytes, producing matrix that obliterates the canal lumen. This transformation does not negatively impact adjacent cartilage. In maturity, epiphyseal growth cartilage is replaced by bone, and cartilage canals disappear completely (Figure 3).

4. Etiological factors contributing to the development of osteochondritis dissecans

Osteochondrosis (OC) is considered a multifactorial disorder, with several key factors implicated in its development, including rapid growth, genetic predisposition, anatomical characteristics, trauma, dietary imbalances and vascular deficiencies.

4.1. Rapid musculoskeletal growth

In horses, increased circulating insulin levels and reduced thyroxine levels, both influenced by high-energy diets, are thought to inhibit chondrocyte maturation and hypertrophy. These hormonal changes affect the chondrocytes located around cartilage canals, potentially leading to persistent cartilage cores that eventually undergo necrosis due to biochemical factors at the transition zone between cartilage and bone. However, some studies contradict this theory, suggesting that OC lesions exhibit distinct areas of necrotic chondrocytes sharply demarcated from the surrounding epiphyseal cartilage. The precise role of rapid growth in OC remains unclear, as lesions tend to appear focally rather than systemically, making a direct correlation challenging.

4.2. Genetic influence on OCD development

Variations in OC prevalence among different horse breeds suggest a strong hereditary component. Genetic studies indicate that osteochondrosis  is a polygenic trait, with estimated prevalence rates ranging from 7% to 64% in sport horse breeds. However, the specific genetic traits contributing to OC and their interaction with environmental factors remain uncertain.

4.3. Anatomical factors

Anatomical variations play a role in OC development, though they are often genetically linked. However, due to the difficulty of consistently measuring anatomical traits and their changes as OC progresses, it remains challenging to determine their exact contribution.

4.4. Physical exercise and OCD lesion formation

Exercise is a crucial factor in cartilage adaptation and the development of joint structure during early growth, particularly in the first year of life. Since OC lesions appear during the same period when cartilage composition matures, researchers hypothesize that exercise intensity could influence OC development.

Preliminary studies on controlled exercise in sport horse foals (3-24 months) reported an OC incidence of 6% in highly exercised groups and 20% in less exercised groups. However, these findings were confounded by simultaneous nutritional studies. Additional research indicated a potential decrease in OC lesions in foals undergoing structured exercise, though the results were inconclusive.

A study by Wilke found that foals subjected to intense exercise developed OC lesions in the distal sagittal ridge of the metacarpus and metatarsus (metacarpophalangeal and metatarsophalangeal joints), but not in the tarsocrural joint. This suggests that exercise may contribute to OCD development, but it is not a primary causative factor.

4.5. Role of trauma in OCD development

Trauma has long been proposed as a primary cause of osteochondrosis  across species. The fact that OC lesions occur in biomechanically stressed joint regions supports this theory. Additionally, higher mechanical stress appears to correlate with increased lesion severity.

However, the role of trauma in OC pathogenesis may vary depending on the lesion phase. Mild trauma can convert subclinical osteochondrosis manifesta into osteochondritis dissecans, even when impact forces are minimal. Despite this, there is no evidence that acute trauma alone initiates primary OC lesions. The traumatic hypothesis also fails to explain the bilateral symmetry seen in OC lesions.

4.6. Breed influence on OCD incidence

Osteochondrosis occurs across multiple horse breeds, though prevalence varies. Studies on Swedish Trotters report an OC incidence of 10.5% in the tarsocrural joint, compared to 12% reported by Schougaard et al. and to 26% by Hoppe and Philipsson. In Standardbred Trotters, Alvarado et al. found a 35% OC incidence in the femoropatellar and metacarpophalangeal joints in the US.

In a French study on 1180 horses, the tarsocrural OC incidence was 13.3%.

Research in Germany found OC rates of 19.5% in the metacarpophalangeal joint, 11.1% in the tarsocrural joint, and 7.2% in the femoropatellar joint. Annually, an estimated 20,000-25,000 foals in Northwestern Europe develop OC lesions.

Osteochondrosis is rare in ponies, with a study on 80 wild horses reporting an OC incidence of 2.5% in the tarsocrural joint and 0% in the femoropatellar joint.

4.7. Nutritional factors in OCD pathogenesis

Dietary imbalances, including calcium-phosphorus imbalances, copper deficiencies, excess zinc, and vitamin deficiencies (A, D, C, biotin), have been implicated in osteochondrosis . Copper deficiency, in particular, is associated with OC lesions in horses.

Studies suggest that copper plays a key role in collagen synthesis via the enzyme lysyl oxidase, which is copper-dependent. High zinc and cadmium levels may inhibit copper absorption, affecting cartilage integrity. However, research has failed to provide conclusive evidence that copper deficiency alone causes osteochondrosis .

4.8. Vascular deficiencies and OCD development

Early studies suggested that cartilage canals in the epiphysis primarily function to nourish cartilage and that their presence might delay ossification. Extensive research in pigs revealed that vascular disruptions in cartilage canals lead to localized chondronecrosis, suggesting a potential link between vascular defects and OC lesions.

Artificial vascular deprivation experiments confirmed that cartilage necrosis resulted in OC-like lesions, reinforcing the idea that vascular failure may contribute to osteochondrosis – Figure 4.

However, later studies examining cartilage canal regression found no consistent link between normal regression patterns and OC. This led to the conclusion that osteochondrosis is not simply a failure of endochondral ossification, nor is it solely caused by systemic growth factors.

Instead, OC is now thought to result from damage to specific cartilage canals, particularly at vascular anastomoses that connect to the bone marrow. While cartilage canals in young horses resemble those in pigs, the chondronecrotic lesions observed in swine are rare in horses, suggesting species-specific differences in OC pathogenesis.

5. Molecular mechanism of osteochondrosis

A deeper understanding of the molecular mechanisms underlying osteochondrosis (OC) is crucial for improving its diagnosis and prevention. In recent years, extensive research has focused on the behavior of chondrocytes and the composition of the extracellular matrix in equine OC. Lilich et al. identified changes in proteoglycan composition within osteochondral fragments but were unable to determine whether these changes were primary or secondary to the disease. This remains a challenge, as clinical samples collected during surgical interventions often do not reflect the initial stages of the disease. Studies have therefore focused on comparing normal and abnormal cartilage to examine the expression of different collagen types (II, VI, X) and growth factors (TGF-β, IGF-I, IGF-II), which play a key role in cartilage development and maturation.

Chondrocyte metabolism and extracellular matrix alterations

Research indicates differences in cellular activity between normal and diseased tissues, with increased chondrocyte activity observed around cartilage cell clusters (chondroid cores) in early OC cases. This heightened metabolic activity was suggested by Van den Hoogen et al. as a secondary process, representing an attempt at regeneration rather than a primary cause. Further studies on subchondral bone have investigated the role of bone morphogenetic enzymes, lipid membrane composition, and cellular components, highlighting their involvement in cartilage defect formation.

Elevated matrix metalloproteinase (MMP) levels have been reported in copper-deficient horses with clinical osteochondrosis, implicating changes in collagen metabolism as a contributing factor in the disease’s molecular mechanism. The Cambridge research group conducted detailed studies on the distribution of cathepsins B, D and L in normal and osteochondrotic cartilage, revealing physiological differences and a notable increase in cathepsin B activity in the clonal chondrocytes within osteochondrosis lesions.

Al Hizab et al. further demonstrated increased gelatinase activity in osteochondrotic cartilage. The elevated collagen turnover in OC cartilage is reflected in the accumulation of collagen-degrading enzymes, detectable in synovial fluid. Laverty et al. identified increased levels of C-propeptide of type II collagen in synovial fluid of OC-affected horses, accompanied by a decrease in aggrecan epitopes. These findings indicate alterations in aggrecan structure and collagen turnover, later confirmed by an in vivo study, which suggested collagen degradation as a primary process in osteochondrosis.

Collagen biomarkers in OC diagnosis

Bilinghurst et al. demonstrated that OC presence could be predicted by detecting collagen markers in blood serum. Additional studies revealed a significant increase in MMP-1 levels, as well as hydroxyproline-collagen degradation in synovial fluid, in OC-affected horses compared to healthy controls. These findings further confirmed post-translational modifications in type II collagen within early OC lesions. Overall, evidence strongly suggests that collagen metabolism alterations play a critical role in OC pathogenesis, though it remains unclear whether these changes are a primary cause or a secondary consequence of the disease.

The role of growth factors in OC pathogenesis

Parathyroid hormone-related peptides (PTHrP) and Indian hedgehog (Ihh) are key regulators of cartilage differentiation and hypertrophy in the growth plate. Their influence is mediated by bone morphogenetic proteins (BMPs), leading to the hypothesis that these molecules may also be involved in the differentiation of articular-epiphyseal cartilage complex (AECC) chondrocytes and thus contribute to OC pathogenesis. Studies have confirmed a significant increase in PTH protein levels and mRNA expression in OC-affected cartilage, whereas no changes were observed in Ihh expression.

These findings highlight the complex molecular interactions governing OC development, emphasizing the need for further biomolecular research to clarify whether collagen metabolism changes and growth factor dysregulation are primary triggers or secondary responses in OC pathogenesis.

6. The diagnosis of OCD

According to Jörg Auer, the typical OCD patient is a foal under 1 year of age, presenting with joint effusion in the tibiotarsal or femoropatellar joint, recently noticed by the owner. The horse is usually not lame, and radiographic examination often reveals intraarticular cartilage fragments or irregularities in the articular surfaces.

The age of onset varies, although most cases involve young animals. In severe cases, particularly in the stifle joint, clinical signs may appear as early as six months. OCD can also become apparent when horses begin training, as joint stress from athletic activities exacerbates symptoms. The age at which this occurs depends on the horse’s discipline. For instance, Thoroughbreds and Standardbreds typically show symptoms earlier than other breeds.

6.1. Common sites of OCD lesions

Osteochondritis dissecans is most frequently diagnosed in the tarsal and metacarpophalangeal joints, but it has been reported in nearly all diarthrodial joints. In an experimental study on Thoroughbred foals, positive stallions and partially affected mares were bred to increase OCD prevalence. At 5 months of age, 24 foals were euthanized, and all joints were examined macroscopically and microscopically.

• Tarsocrural joint: most affected (approximately two lesions per animal).
• Femoropatellar and cervical intervertebral joints: approximately one lesion per animal.
• Metatarso (falangeal) and carpal joints: approximately 0.4 lesions per animal.
• Humeroradial joint: 0.2 lesions per animal.
• Scapulohumeral joint: 0.04 lesions per animal.

Although this study artificially increased OCD prevalence, the relative distribution of lesions matched clinical observations in Thoroughbreds. The site of OCD lesions varies by breed, with femoropatellar OCD being common in Standardbreds, whereas tarsocrural OCD is more frequent in Thoroughbreds.

6.2. Typical locations of OCD lesions

Osteochondritis dissecans lesions consistently occur in specific areas within a joint.

• Tarsocrural joint: cranial and distal intermediate ridge of the tibia, lateral trochlear ridge, medial malleolus of the tibia.
• Femoropatellar joint: medial trochlear ridge of the femur.
• Less common sites: lateral trochlear ridge, trochlear groove, distal patella.
• Subchondral bone cysts: medial femoral condyle.
• Metacarpophalangeal and metatarsophalangeal joints: dorsal margin of the sagittal ridge.

6.3. Bilateral occurrence and radiographic recommendations

• OCD is often bilateral in the tarsocrural and femoropatellar joints, as well as in all four metacarpophalangeal/metatarsophalangeal joints.
• Despite bilateral involvement, the clinical signs may be unilateral.
• More than 50% of clinically affected horses have bilateral OCD in the tarsocrural or femoropatellar joints, so radiographic examination of the opposite limb is recommended.
• Some joints are less likely to have bilateral involvement. A study on 225 horses with tarsocrural OCD found that only eight cases had lesions in other joints, so routine whole-body radiography is unnecessary unless clinical signs suggest additional locations.

6.4. Clinical signs and radiographic findings

• Joint effusion is the most common clinical sign and may lead to lameness, especially in cases with large lesions detected on radiographs.
• Lameness is more common in femoropatellar OCD than in tarsocrural OCD, and occurs when bone fragments detach or partial fragmentation is visible radiographically.
• Other subtle radiographic signs include irregularities of the subchondral bone contour, surface flattening, or mild depression.
• Small radiographic changes should be interpreted by an experienced radiologist, as they may only represent mild cartilage defects.

However, radiographic severity does not always correlate with findings from arthroscopy or necropsy. Many cases reveal more extensive cartilage damage than radiographs suggest, or cartilage lesions without subchondral bone changes, making them radiographically undetectable.

Advanced imaging, such as MRI, provides a better assessment of lesion severity, but its clinical and economic feasibility is limited, particularly for the femoropatellar joint.

6.5. Imaging diagnosis

Radiographic examination

Radiology has evolved significantly, with increasingly powerful and precise equipment improving veterinary diagnostics).

• Intraarticular fractures are identified by disruptions in the joint surface.
• Small fractures or cartilage damage may go undetected if displacement is minimal, but slight “step” misalignments may indicate a fracture.
• Chip fractures at the joint margins must be distinguished from ectopic mineralization or separate ossification centers, though this is sometimes difficult.

• discrete osteochondral fragments
• irregular joint surface contours
• flattening or depression of the articular surface
• subchondral bone sclerosis
• secondary joint remodeling.

Some lesions may be clinically insignificant, but should be interpreted alongside clinical signs. In some cases, lesions may gradually remodel and become sclerotic. Clinical signs are usually observed in horses under 3 years old, though some remain asymptomatic until later.

Ultrasonographic examination

Ultrasound imaging was introduced to veterinary medicine in the 1980s, initially used for reproductive examinations with 5-MHz rectal probes. While early ultrasound systems were not ideal for musculoskeletal imaging, innovative equine veterinarians adapted them for evaluating flexor tendons.

With advancements in ultrasound technology, linear probes have been optimized for musculoskeletal evaluations. Ultrasonography is now the best imaging modality for soft tissues in horses, playing a crucial role in diagnosing:

• flexor tendons, suspensory ligaments, sesamoidean ligaments and accessory ligaments
• subcutaneous tissue, peritendinous tissue, blood vessels, and cortical bone contours.

Ultrasound is particularly useful for monitoring and guiding tendon and ligament healing.

In addition to soft tissue assessments, ultrasono­graphy helps diagnose:

• long bone fractures
• osteitis/osteomyelitis
• cartilage fragments in OCD
• foreign body penetration
• joint infections.

It is also used intraoperatively to assist with surgical procedures.

Diagnosis using inertial sensors

Inertial sensors attached to the horse’s body provide an objective kinematic evaluation of lameness, making them one of the most reliable diagnostic tools for detecting subtle movement asymmetries. These sensors capture body motion in real time, transmitting data wirelessly to a computer, which makes them ideal for field conditions.

For clinical relevance, inertial sensors must meet several criteria:

• They should be small and lightweight to avoid interfering with normal limb motion.
• The collected data must be more sensitive than the human eye and processed using high-quality digital support for accurate representation.
• The signal transmission range should be sufficient for evaluating movement in a typical clinical or field setting.
• Data collection and analysis should be fast and easy to interpret, providing meaningful quantification of lameness.

Several companies produce inertial sensor systems, with some of the most commonly used being:

• EquuSense Equine Sensor (EquuSys Inc., USA) – a system with multiple sensors, a laptop, and dedicated software that tracks position, speed, acceleration, orientation and rotation in relation to the horse or a fixed reference point. It supports 8 to 18 sensors, depending on the model.
• Lameness Locator – developed by the University of Missouri in collaboration with the Hiroshima Institute of Technology, Japan, this system includes three wireless inertial sensors, two accelerometers, and a gyroscope attached to the head, right forelimb and pelvis. The system transmits data to a tablet with a 150 m signal range.

The lameness locator detects vertical trunk acceleration using:

• the head accelerometer for forelimb lameness
• the pelvis accelerometer for hindlimb lameness.

It analyzes asymmetry between the horse’s right and left sides, converting vertical acceleration data into position signals via an error-correcting double integral.

These signals are further broken down into harmonic components and random motion data.

Results are displayed as diagrams, with each ray representing asymmetric head movement amplitude. The distribution of rays in quadrants indicates the location and timing of lameness.

Lameness quantification is based on four values that describe the severity and symmetry of head and pelvis movements during forelimb and hindlimb strides (Figure 5).

A forelimb lameness threshold (A1/A2) above 0.50 indicates a clinically significant lameness.

For hindlimb lameness, the threshold is 0.17, as hindlimb movement is analyzed relative to pelvic motion.

Diagnosis via arthroscopy

While arthroscopy is widely known for its surgical applications, its diagnostic potential is often underappreciated. Traditional diagnostic methods, such as clinical examination, radiography (with or without contrast agents) and synovial fluid analysis, have limitations, particularly when evaluating cartilage damage. The value of arthroscopy in equine joint evaluation was first demonstrated in 1978. Its effectiveness in human orthopedic surgery has been well established.

Arthroscopy is a complementary diagnostic tool, not a replacement for radiography or other imaging techniques. Studies by Joyce & Mankin (1983) emphasize the importance of radiographic evaluation before and after arthroscopy to ensure comprehensive joint assessment.

Arthroscopy is particularly useful for evaluating:

• synovial membranes
• articular cartilage
• intraarticular ligaments
• menisci (especially in the stifle joint).

In equine medicine, arthroscopic evaluation of the femorotibial joint has provided significant insights into joint pathology, leading to major advancements in both diagnosis and surgery.

Clinical applications of arthroscopy

Arthroscopy is especially valuable when other diagnostic methods fail to provide a definitive diagnosis. Some conditions that benefit from arthroscopic assessment include:

• cruciate ligament ruptures
• medial intercarpal ligament injuries
• meniscal tears
• osteochondral fragmentation (undetectable on radiographs)
• subchondral bone defects
• cartilage lesions.

By allowing the direct visualization of joint structures, arthroscopy offers a superior level of diagnostic accuracy, making it an indispensable tool in evaluating equine joint disorders, particularly OCD lesions.

7. Treatment strategies

The use of hyaluronic acid in OCD therapy

Hyaluronic acid (HA) is a glycosaminoglycan composed of D-glucuronic acid and N-acetyl-D-glucosamine disaccharide units. It is a key component of articular cartilage, contributing to the viscoelastic properties of synovial fluid and serving as the primary lubricant for soft synovial tissues. Initially, HA supplementation was introduced to restore synovial fluid viscosity, but research has since shown that HA has a broad pharmacological spectrum, making it effective in managing clinical symptoms.

Hyaluronic acid possesses direct analgesic effects, reducing the sensitivity of articular nerve endings. Additionally, it exerts anti-inflammatory properties both through physical filtration/exclusion and pharmacological inhibition of inflammatory cells and mediators, further contributing to its pain-relieving effects. The clinical response to HA treatment varies between cases, but in some horses the improvement is remarkable.

Several studies have investigated whether HA modifies the disease course, but its exact mechanism of action remains unclear. HA is known to bind to specific cell membrane receptors, primarily CD44, which is believed to mediate many of its biological effects. The most significant of these effects appears to be cartilage protection, preventing matrix degradation caused by IL-1 and other inflammatory mediators.

It has been suggested that high molecular weight HA (>1000 kDa) has superior chondroprotective effects, although this remains theoretical. While in vitro studies indicate that molecular weight affects HA’s biological activity, its in vivo effects remain uncertain. Current evidence suggests that HA formulations with molecular weights between 500 and 2000 kDa offer optimal therapeutic benefits.

In equine medicine, hyaluronic acid appears to be more effective in treating early joint lesions rather than chronic ones, where outcomes can be disappointing. This observation aligns with human clinical experience, where patients with mild radiographic changes respond better to HA therapy than those with advanced joint degeneration. Despite high treatment costs, administering 4-5 injections at 7-14-day intervals has been shown to yield optimal results.

The use of corticosteroids in intraarticular therapy for OCD

Among all available medications for equine arthritis, intraarticular corticosteroids offer the most potent anti-inflammatory effects. They have been a mainstay of arthritis treatment for over 50 years, not only due to their general anti-inflammatory properties but also because they inhibit the synthesis and release of inflammatory mediators that contribute to cartilage degeneration and associated symptoms.

Corticosteroids, like NSAIDs, primarily reduce pain by inhibiting prostaglandin synthesis, specifically through the suppression of phospholipase A2 and COX-2, both of which are essential enzymes in the arachidonic acid cascade.

Studies have confirmed that corticosteroids can alter the course of arthritis by strongly inhibiting cytokines involved in cartilage degeneration. At low concentrations, corticosteroids prevent the expression of IL-1 and tumor necrosis factor-alpha (TNF-α), two key mediators of cartilage degradation. Additionally, they inhibit matrix metalloproteinases and other cartilage-degrading enzymes. High doses have been shown to modify disease progression without significantly compromising chondrocyte health.

However, intraarticular corticosteroid use remains controversial due to concerns that pain relief may lead to increased joint use, potentially accelerating cartilage degeneration. Some studies have reported adverse effects on chondrocyte metabolism, particularly at high corticosteroid concentrations, leading to reversible changes in cartilage matrix synthesis. That said, the corticosteroid doses required to induce harmful effects are much higher than those needed to inhibit cartilage degradation mediators. While repeated high-dose injections can lead to complications, the actual clinical relevance of corticosteroid-induced arthropathy is debatable, as studies suggest it is rare.

Clinicians now favor lower corticosteroid doses, balancing therapeutic benefits with minimal risk. For instance, methylprednisolone acetate doses have been reduced to 10-40 mg per joint, compared to the previously recommended 120-200 mg per joint. It is important to note that all intraarticular injections carry a risk of septic arthritis, and with corticosteroids, the symptoms may be delayed due to their strong anti-inflammatory effects.

In conclusion, corticosteroid injections provide remarkable symptom relief, and when used correctly, they do not compromise joint function or long-term health.

The use of stem cells in intraarticular therapy for OCD

Bone marrow is typically harvested from the sternum in standing horses or under general anesthesia. The fourth sternebra is preferred due to its relatively flat surface, which facilitates trocar insertion and allows for adequate marrow collection while minimizing the risk of deviations that could injure the myocardium. The third sternebra provides greater myocardial protection, but its angled surface increases trocar deviation risks. The fifth sternebra has a flat surface, making trocar placement easier, but yields less marrow.

Once contact with the bone is established (~4 cm deep), the trocar is advanced another 2 cm using a rotational motion. Approximately 20 ml of bone marrow is aspirated into a 50 ml syringe, with moderate suction applied. The sample is darker than blood and has a fatty consistency. Microscopic examination ensures quality control by assessing stem cell density and identifying nucleated, multilobed cells while differentiating them from contaminating blood cells.

Stem cell administration techniques

Three techniques are currently available:

• Direct bone marrow injection
• The marrow is injected immediately into the lesion site.
• The volume varies between a few ml to a maximum of 10 ml.
• Placement is confirmed by ultrasound, and no adverse effects were reported in 47 cases.
• Horses undergo eight days of stall rest, followed by controlled exercise until returning to full training at nine months.

Cultured mesenchymal stem cells (MSCs)

• Bone marrow is collected and shipped to a laboratory within 48 hours.
• Cells are cultured for six weeks to reach 10 million stem cells per 2 ml sample.
• Cells are then injected into the lesion site.

• Bone marrow is processed via centrifugation (3200 RPM for 5 minutes) to enrich platelet and stem cell content.

The results vary, with 50-80% of cases showing improvement and minimal adverse effects.

Alternative sources of stem cells include umbilical cord blood, which is considered high quality, though its proliferation rate is harder to control. Adipose tissue-derived stem cells are another option, but their isolation is more challenging, and they are less pluripotent than bone marrow-derived stem cells.

8. Prevention and future directions

8.1 Prevention strategies

Although osteochondritis dissecans (OCD) has a multifactorial etiology, preventive strategies can significantly reduce its incidence. Given the strong genetic predisposition, selective breeding programs should focus on reducing hereditary susceptibility.

Key preventive measures include:

• Breeding selection
  • Avoid breeding horses with a history of OCD to reduce genetic predisposition.
  • Implement radiographic screening for potential breeding stock.
• Nutritional management
  • Ensure balanced mineral intake, particularly calcium, phosphorus, copper and zinc, as deficiencies or imbalances have been implicated in cartilage development disorders.
  • Avoid excessive energy intake, which may promote rapid growth and abnormal cartilage maturation.
• Exercise and controlled growth
  • Moderate, controlled exercise during early life helps promote healthy musculoskeletal development.
  • Avoid intensive training or high-impact activities in young horses, as excessive biomechanical stress may contribute to lesion development.
• Early veterinary surveillance
  • Routine clinical and radiographic monitoring of foals and yearlings can identify early-stage lesions, allowing for timely intervention.

8.2. Future directions in OCD research and treatment

Advances in regenerative medicine, molecular research and imaging techniques continue to shape the future of OCD diagnosis and treatment. Key areas of development include:

• Gene therapy and molecular interventions
  • Ongoing research aims to identify specific genetic markers associated with OCD susceptibility.
  • Molecular therapies targeting inflammatory pathways (e.g., IL-1 and TNF-α inhibitors) may provide new treatment options.
• Advanced imaging techniques
  • Improved MRI and CT scanning allow for earlier and more accurate lesion detection compared to traditional radiography.
• Biologic therapies and regenerative medicine
  • Stem cell therapy continues to evolve, with ongoing studies investigating optimal cell sources and administration techniques.
  • Growth factor-based treatments, such as IGF-1 and TGF-β, show potential for stimulating cartilage repair.
• Personalized medicine and artificial intelligence
  • AI-driven diagnostic models could improve early detection and prognosis predictions based on imaging and clinical data.
  • Personalized treatment protocols using genetic and biomarker-based approaches may help tailor OCD management to individual horses.

9. Conclusions

Osteochondritis dissecans remains one of the most significant orthopedic conditions affecting young horses, with implications for performance, welfare, and economic impact in the equine industry.

While the exact pathogenesis is not fully understood, genetics, nutrition, trauma, vascular deficiencies and biomechanical stress play key roles in its development.

Diagnostic advancements, including radiography, ultrasonography, MRI and inertial sensor-based motion analysis, allow for earlier detection and better monitoring of OCD lesions. Treatment strategies have evolved to incorporate hyaluronic acid, corticosteroids, and stem cell therapy, with regenerative medicine offering promising future alternatives.

Prevention remains the most effective long-term approach, focusing on selective breeding, proper nutrition, controlled exercise and early veterinary surveillance. Future research should continue to explore genetic, molecular and regenerative therapies, aiming for more targeted and effective treatment options.

With ongoing advancements in diagnostics, treatment and preventive care, the prognosis for horses affected by osteochondritis dissecans continues to improve, paving the way for better long-term joint health and performance longevity.   

Autor corespondent: Cristian-Mihăiță Crecan E-mail:  cristi_crecan@yahoo.com

All authors had equal contributions

CONFLICT OF INTEREST: none declared.

FINANCIAL SUPPORT: none declared.

This work is permanently accessible online free of charge and published under the CC-BY.