The Role of Persistent Inflammation in the Pathogenesis of Infected Nonunion: A Narrative Review.

INTRODUCTION

Infected Nonunion is a challenging condition that arises from infections at the fracture site, causing persistent inflammation and preventing proper healing of the fracture ends. This condition not only causes significant physical suffering but also imposes a heavy economic burden on patients. Despite the recognized link between Infected Nonunion and infection, the mechanisms underlying its occurrence and development remain incompletely understood. Recent studies have highlighted the close association between inflammatory factors and Infected Nonunion, suggesting that inflammation plays a pivotal role in its pathogenesis. However, a narrative review and summary of relevant literature are lacking. Therefore, this study aims to clarify the inflammatory mechanisms of Infected Nonunion and identify potential therapeutic targets.

METHODS

A comprehensive literature search was conducted to identify relevant domestic and international studies on the inflammatory mechanisms of Infected Nonunion. The search included databases such as PubMed using keywords related to Infected Nonunion, inflammation, and mechanisms. The selected studies were critically reviewed and summarized to extract key information on the inflammatory pathways, cytokines, and other relevant factors involved in Infected Nonunion.

RESULTS

The review identified several key inflammatory mechanisms that contribute to the development of Infected Nonunion. These include the activation of inflammatory cells, the release of inflammatory cytokines and chemokines, and the disruption of normal fracture healing processes.

CONCLUSIONS

This narrative review elucidates novel perspectives on the inflammatory mechanisms in infected nonunion, with persistent inflammatory response triggered by pathogenic infection representing the core pathological process. The findings provide theoretical foundations for future research and therapeutic strategies, potentially facilitating the development of more effective treatments for infected nonunion. Targeted modulation of these inflammatory pathways may optimize fracture healing outcomes and alleviate the clinical burden of this condition.