Related Experiment Video
Updated: Apr 3, 2026
In vivo Structural Assessments of Ocular Disease in Rodent Models using Optical Coherence Tomography
Published on: July 24, 2020
A Systematic Review of Animal Models of Trochlear Dysplasia Development: Rationalization for a Large-Animal Model
Alexander Gerick1,2, Jacob Jordan2,3, Marina Santos4
1Philadelphia College of Osteopathic Medicine, Philadelphia, PA.
Background:
Trochlear dysplasia is the leading risk factor for patellofemoral instability, but its development in humans is poorly understood. Animal models provide an avenue for improving our understanding of this condition, yet they face several limitations in replicating human anatomy. This systematic review sought to evaluate existing animal models of trochlear dysplasia, highlighting their effectiveness, limitations, and translational relevance.
Methods:
A systematic review was conducted following PRISMA guidelines. PubMed, Embase, and Scopus were searched for studies that induced trochlear dysplasia in animals. Eligible studies included control groups and reported radiographic measurements of trochlear dysplasia, including sulcus angle and depth. These outcomes were assessed across different species, interventions, and follow-up periods.
Results:
We identified 18 studies demonstrating the induction of trochlear dysplasia in three species (rabbit, rat, and mouse). Dysplasia was produced with a variety of operative and nonoperative interventions. Animal models consistently demonstrated progressive dysplastic trochlear changes over time. The severity and rate of trochlear dysplasia varied by species and intervention type. Follow-up periods ranged from 1 month to 1 year in rabbit models, 3 weeks to 3 months in rat models, and 2 weeks to 1 month in mouse models. Statistically significant changes were observed as early as 3 months in rabbit models and 6 weeks in rat and mouse models. Few studies have conducted longitudinal follow-ups beyond their initial establishment of trochlear dysplasia. Only early patellar reduction surgery prevented trochlear dysplasia.
Conclusions:
Trochlear dysplasia has been reliably induced using a variety of small-animal models. Early patellar reduction was observed to prevent dysplasia, but longitudinal follow-up is limited, and the severity of dysplastic changes is variable. Development of a large-animal model with slower skeletal maturation may provide greater translational fidelity to human trochlear development and permit increased understanding of potential interventions to reverse dysplasia development.
Level Of Evidence:
Level III.
