The use of polypropylene mesh in thoracoplasty: an experimental and clinical study

Abstract

Relevance. Thoracoplasty is an effective way to close the cavity of destruction of the lung tissue and achieve clinical recovery in case of fibro-cavernous pulmonary tuberculosis. A promising direction of creating selective collapse in thoracoplasty is the use of synthetic mesh implants.
 The purpose of the study was to assess the effect of synthetic implants from the “Surgipro" polypropylene mesh on the inflammatory and reparative reaction in thoracoplasty.
 Materials and methods. The work was performed on male Wistar rats weighing 250±50 grams (n=12). The “Surgipro” polypropylene mesh was implanted on the right posterolateral surface of the chest (n=9). As control, the material was taken from intact rats (n=3), which were kept in the same conditions as experimental animals. The study material was biopsy specimens of the muscular aponeurotic scar of the posterolateral surface of the chest of rats. The cellular composition and total number of mast cells were determined. A clinical study was conducted on 26 cases of thoracoplastic with the use of polypropylene mesh in the pulmonary-surgical department of the Seaside regional antituberculous dispensary in Vladivostok.
 Results. During the experimental study, it was recorded that the implant used in the reconstruction of the chest has a pronounced reactogenicity from the first day, which manifests itself as a local inflammatory reaction with the concentration of mast cells. The population of mast cells progressively declined by the 30th day, while an increase in the number of macrophages and fibroblasts was observed with the advent of giant multinuclear cells of foreign bodies. On the 30th day after the operation, a widespread post-inflammatory reactive fibrosis and angiomatosis with chronic productive inflammation was observed in the experiment. In clinical observation, the resulting inflammatory reaction around the endoprosthesis spreads to the surrounding tissues and lung, which contributes to the formation of pronounced pulmonary fibrosis and restriction of a specific process.