Elbow dysplasia remains the most common cause of forelimb lameness in large-breed dogs, yet the term itself encompasses three distinct developmental abnormalities that many practitioners still conflate. After examining thousands of radiographs over nearly three decades, I have grown increasingly frustrated with how imprecisely this condition is discussed in breeding circles. The three components require different diagnostic approaches, carry different prognostic implications, and respond differently to surgical intervention.
Defining the Elbow Dysplasia Complex
The International Elbow Working Group (IEWG) formally defined elbow dysplasia in 1990 as an umbrella term encompassing three specific developmental abnormalities: fragmented medial coronoid process (FCP), osteochondritis dissecans of the medial humeral condyle (OCD), and ununited anconeal process (UAP). Wind et al. (1986) first proposed this unified classification, arguing that these conditions share a common etiology rooted in asynchronous growth of the radius and ulna creating abnormal joint mechanics.
What practitioners often fail to appreciate is that these three lesions rarely occur in isolation. Grondalen and Grondalen (1981) documented combined lesions in 42% of affected Rottweilers, while more recent studies by Samoy et al. (2012) found concurrent FCP and OCD in 38% of cases examined arthroscopically. This has significant implications for both diagnosis and treatment planning.
Fragmented Medial Coronoid Process (FCP)
FCP represents the most common component of the elbow dysplasia complex, accounting for approximately 65-70% of all elbow dysplasia diagnoses according to OFA statistics. The medial coronoid process is a small bony projection on the ulna that articulates with the medial humeral condyle. In affected dogs, this process fails to fuse properly with the ulna or subsequently fragments due to abnormal loading forces.
FCP Diagnostic Criteria
- Radiographic signs often subtle; may require CT confirmation
- Sclerosis of the trochlear notch visible on ML views
- Blunting or irregularity of coronoid apex
- Secondary osteoarthritis on cranial-caudal projections
- Gold standard: arthroscopic visualization
The clinical presentation of FCP typically begins between 4-7 months of age, though dogs may not present for examination until lameness becomes pronounced. Meyer-Lindenberg et al. (2006) demonstrated that 87% of dogs with FCP showed radiographic evidence of secondary osteoarthritis by 12 months of age, emphasizing the importance of early screening. The heritability of FCP has been estimated at 0.27-0.45 across different breed populations (Malm et al., 2008).
Research Note: Radiographic Sensitivity
Carpenter et al. (1993) found standard radiography detected only 60-70% of FCP lesions confirmed by arthroscopy. Moores et al. (2008) improved detection to 85% using specific oblique projections, but CT imaging remains superior with 95%+ sensitivity.
Osteochondritis Dissecans (OCD)
OCD of the medial humeral condyle occurs when a focal area of articular cartilage and subchondral bone fails to ossify normally, creating a flap of cartilage that may partially or completely detach into the joint. This condition accounts for approximately 20-25% of elbow dysplasia cases and has a reported heritability of 0.25-0.35 (Guthrie and Pidduck, 1990).
The pathophysiology involves disruption of endochondral ossification, likely resulting from a combination of genetic predisposition, rapid growth, and nutritional factors. Ytrehus et al. (2007) demonstrated that cartilage canals fail to regress normally in affected areas, creating focal regions of ischemic necrosis that progress to the characteristic lesions.
OCD Radiographic Features
- Flattening or irregularity of medial humeral condyle
- Subchondral bone defect visible on flexed ML view
- Possible mineralized cartilage flap in joint space
- Associated osteophyte formation
- Best visualized with 15-degree supinated oblique projection
Clinical onset typically occurs between 4-8 months, coinciding with the period of most rapid skeletal growth. Males are overrepresented at a ratio of approximately 2:1 (LaFond et al., 2002). Bilateral involvement occurs in 20-50% of cases, mandating radiographic evaluation of both elbows regardless of clinical presentation.
Ununited Anconeal Process (UAP)
UAP occurs when the anconeal process fails to fuse with the ulnar metaphysis by the expected age of ossification (approximately 16-20 weeks in most breeds). This creates joint instability and progressive osteoarthritis. UAP accounts for 10-15% of elbow dysplasia diagnoses and demonstrates the highest heritability of the three components, estimated at 0.45-0.55 (Beuing et al., 2000).
The German Shepherd remains disproportionately affected, with UAP prevalence 3-4 times higher than in other breeds of similar size. Sjostrom et al. (1995) proposed this relates to breed-specific differences in the timing of anconeal ossification combined with the characteristically upright pastern angle that increases anconeal loading.
UAP Diagnostic Approach
- Definitive diagnosis requires flexed lateral radiograph
- Visible radiolucent line between anconeal process and olecranon
- May show displacement or rotation of unfused process
- Screening unreliable before 20 weeks of age
- Bilateral evaluation essential (30-40% bilateral)
Diagnostic Caution
The anconeal process ossifies from a separate center that normally fuses by 16-20 weeks. Radiographic evaluation before this age will show a normal radiolucent line that should not be misinterpreted as UAP. Always confirm patient age before diagnosis.
Elbow Incongruity: The Fourth Component?
Some investigators, notably Samoy et al. (2006), have argued for including elbow incongruity as a fourth component of elbow dysplasia. Incongruity refers to malalignment between the radius and ulna that creates abnormal stress distribution across the joint surfaces. The IEWG has resisted formal inclusion, as incongruity likely represents the mechanical precursor to the three recognized lesions rather than a distinct pathology.
Regardless of classification debates, incongruity has significant clinical relevance. Preston et al. (2000) demonstrated that even 2mm of radio-ulnar length discrepancy significantly alters joint contact mechanics. This finding explains why seemingly mild incongruity can progress to severe secondary osteoarthritis and informs surgical decision-making regarding ulnar osteotomy procedures.
Genetic Considerations for Breeders
The polygenic inheritance pattern of elbow dysplasia complicates breeding decisions. Maki et al. (2000) estimated that genetic factors account for 30-45% of phenotypic variation, with the remainder attributed to environmental influences including nutrition, exercise, and growth rate. This moderate heritability means that screening and selective breeding can reduce population prevalence, but progress will be gradual.
| Component | Prevalence | Heritability | Bilateral Rate |
|---|---|---|---|
| FCP | 65-70% | 0.27-0.45 | 50-60% |
| OCD | 20-25% | 0.25-0.35 | 20-50% |
| UAP | 10-15% | 0.45-0.55 | 30-40% |
Data synthesized from OFA registry and European breed-specific studies (1990-2024)
The practical implication for breeding programs is that estimated breeding values (EBVs) based on offspring and sibling data provide more accurate genetic assessment than individual phenotype alone. The Finnish Kennel Club and Swedish Kennel Club have implemented EBV-based systems that have demonstrated measurable population-level improvements over 15-year periods (Malm et al., 2008).
Related Database Resources
- Elbow Grading Systems Comparison - Understanding how different registries score these components
- Breed Prevalence Statistics - Component-specific rates by breed
- Screening Protocol Recommendations - Optimal timing and technique for detection
- The Herding Gene - Comprehensive genetic resources for herding breeds
Conclusion
Understanding elbow dysplasia requires recognizing it as a complex of related but distinct pathologies rather than a single disease entity. Each component has characteristic radiographic features, clinical presentations, and genetic parameters that inform both diagnostic and breeding decisions. The persistent tendency to treat "elbow dysplasia" as a monolithic condition hampers both clinical communication and genetic progress.
For breeders, the key insight is that normal elbow scores indicate absence of radiographically detectable disease at the time of screening, not genetic clearance. Breeding decisions should incorporate pedigree analysis, sibling data, and estimated breeding values where available. The three components share enough genetic overlap that selection against one tends to reduce all three, but progress requires consistent screening across generations and transparent reporting of results.