Introduction: Temporomandibular joint (TMJ) condylar hyperplasia (CH) is a disorder characterized by an increased volume of the condyle, ramus, and mandibular body. CH is a unilateral, self-limiting disorder that results in facial asymmetry and consequent occlusal changes. A comparable pathology has not been described in any other joint. The aetiology of CH remains to be unclear.

The common treatments to correct the asymmetry and malocclusion, is high condylectomy on the affected side followed by orthognathic surgery. While in the last decade self facial remodelling was described avoiding the need for orthognathic surgery.

The mandibular condyle, as most of the skeleton, develops through the endochondral ossification, a process in which vascular endothelial growth factor (VEGF) is an essential mediator.

Our objective is to evaluate the role of VEGF in the pathology of CH by examining its expression in CH human specimens, and in a novel transgenic mouse model.

Materials and methods: The first part of the research examines cases of CH in patients 13–35 years old. Material obtained after condylectomy was fixed, decalcified, embedded in paraffin and serial coronal sections were cut and stained with Haematoxylin–Eosin. In addition, immunohistochemical (IHC) protocols were used to detect VEGF and a variety of bone and cartilage components such as Collagen I and Collagen II.

In addition, we use a novel transgenic mouse model, in which we can induce conditional VEGF over-expression to be locally increased in the skeleton. CH will be monitored in living mice by in-vivo micro-CT scans which will be followed by IHC.

Results:

• a.

  H&E staining of human specimens of resected condyle show a typical hyperplastic area observed in CH.

• b.

  VEGF staining of the healthy area showing presence of VEGF only at the hypertrophic layer while in the pathological area an abundant expression of VEGF was demonstrated throughout all of the layers of the condylar cartilage.

• c.

  In-vivo micro CT scans of Mandibles show the dramatic increase in size of the mandible in Mutant vs. WT mice. When induction of VEGF over expression was stopped the mandible shape returned to normal size. The change in bone volume was quantified.

Conclusion: VEGF has a potential role in the pathogenesis of condylar hyperplasia.