# The Buerger’s rabbit model: a closer step to unravelling thromboangiitis obliterans?

## TL;DR

This study introduces a new rabbit model for thromboangiitis obliterans that closely mimics the human condition, showing similar clinical, radiographic, and histopathological features.

## Contribution

A novel rabbit model of TAO is developed that more accurately reflects the disease's progression and features compared to previous models.

## Key findings

- The TAO rabbit model exhibited ischemia, corkscrew collaterals, and VSMC proliferation similar to human TAO.
- Histopathology showed VSMC origin of intimal thickening and neorevascularization in the MTX-treated group.
- The model demonstrated progressive arterial occlusion and inflammatory cell migration over time.

## Abstract

Thromboangiitis obliterans (TAO) remains clinical challenging due to its rarity and underwhelming management outcomes. This study aimed to describe a novel TAO rabbit model that demonstrates a closer resemblance to TAO.

Thirty-six New Zealand rabbits underwent the surgical implantation of calibrated gelatin sponge particles (CGSPs) into their right femoral artery. The CGSPs were soaked in different solutions to simulate different types of thrombi: normal (NT; normal saline); inflammatory TAO thrombus (TAO; dimethylsulfoxide [DMSO]), and DMSO with methotrexate (MTX). All groups underwent clinical assessment, digital subtraction angiography (DSA) and histopathological analysis at time points day 0 (immediate), week 1 (acute), week 2 (subacute), and week 4 (chronic).

The TAO rabbit presented with signs of ischemia of the right digit at week 4. On DSA, the TAO rabbits exhibited formation of corkscrew collaterals starting week 1. On H&E staining, gradual CGSP degradation was observed along with increased red blood cell aggregation and inflammatory cells migration in week 1. On week 2, disorganization of the tunica media layer and vascular smooth muscle cell (VSMC) proliferation was observed. In the TAO rabbit, migrated VSMCs, inflammatory cells, and extracellular matrix with collagen-like substances gradually occluded the lumen. On week 4, the arterial lumen of the TAO rabbit was filled with relatively-organized VSMC and endothelial cell clusters with less inflammatory cells. Neorevascularization was found in the MTX-treated group.

The novel TAO rabbit model shows a closer resemblance to human TAO clinically, radiographically, and histopathologically. Histological analysis of the IT progression in the TAO model suggests that it is of VSMC origin.

The online version contains supplementary material available at 10.1186/s12959-024-00638-z.