中国修复重建外科杂志最新文献

Objective: To review the research progress related to pain in knee osteoarthritis (KOA).

Methods: A systematic review of relevant research literature at home and abroad in recent years was conducted to analyze the roles played by multi-dimensional factors such as demographics, imaging, serology, bone metabolism, biomechanics, neurological factors, and macrophages in the occurrence and development of KOA pain. The mechanisms of pain induction were expounded and the research directions were prospectively proposed.

Results: The occurrence of KOA pain is a complex process interwoven with multiple factors. Demographic factors such as gender, age, and body weight are closely related to its occurrence and pain degree. Structural changes shown by imaging examinations (such as MRI, ultrasound, and X-ray films) can be used to assess the level of pain. A variety of inflammatory factors released by intra-articular inflammation directly participate in the initiation of pain. Bone metabolic factors can also induce pain by influencing changes in bone density. Biomechanical factors are involved in the pain process by altering the concentrated distribution of joint stress. The various mediators released by the local inflammatory response of the joint trigger hyperalgesia and peripheral nerve sensitization through damage receptors, promoting the conduction and amplification of pain signals. The bidirectional interaction between nerves and joints further intensifies the pain. In addition, the expression of certain ion channels, the mediation and release of pain signals by macrophages and osteoclasts, provide a theoretical direction for in-depth exploration of the microscopic mechanism of KOA pain.

Conclusion: Future research needs to integrate multiple regulatory mechanisms such as biomechanics, inflammation and neural regulation, systematically explore key intervention targets, in order to deepen the understanding of the pain mechanism of KOA and promote the formation of more comprehensive and precise pain diagnosis and treatment plans.

Objective: To review the pathological characteristics of calcaneal fracture malunions and the research progress of surgical treatment, so as to provide a reference for standardized clinical diagnosis and treatment.

Methods: The relevant research literature on calcaneal fracture malunions at home and abroad in recent years was reviewed. The pathological characteristics, imaging manifestations, classification, and the latest surgical treatment strategies of calcaneal fracture malunions were systematically expounded.

Results: Malunion may ensue after calcaneal fractures if conservative treatment fails or surgical intervention is improperly performed, leading to abnormal foot biomechanics and severe functional impairment. Typical pathological changes include three-dimensional morphological disorders of the calcaneus (abnormal width, height loss, and varus-valgus deformity), collapse of the subtalar articular surface accompanied by joint mismatch, secondary joint degeneration, Achilles tendon contracture, and lateral soft tissue impingement syndrome. Given the complex pathological anatomy after malunion, surgical plans should be individually tailored. The clinically used Stephens-Sanders classification and Zwipp-Rammelt classification provide a reliable basis for the accurate selection of treatment modalities. Staged treatments such as subtalar arthrodesis, osteotomy correction, and soft tissue release can effectively improve ankle and foot function.

Conclusion: In recent years, the biomechanical mechanisms, imaging evaluation systems, and reconstructive surgical strategies of calcaneal fracture malunion have become research hotspots. The selection of treatment plans should take into account specific clinical symptoms and morphological changes of the calcaneus, which is crucial for subsequent recovery. In the future, it is necessary to focus on individual differences, promote the integration of diagnosis and treatment, establish evidence-based guidelines, and achieve accurate and long-term deformity correction and functional reconstruction.

Hypospadias is a common congenital external genital structural malformation in the males, where significant deviations in appearance primarily affect the psychosocial health of the entire family during childhood, ultimately harming the patient's social integration, leading to high expectations for normal appearance from the patients and their families. The anatomical abnormalities of hypospadias exhibit considerable individual differences, and the difficulty of surgical repair largely depends on the experience of the surgeon, with high rates of complications and reoperations. Therefore, surgeons' expectations for surgical outcomes are more focused on functional reconstruction and reducing complication rates, creating a gap between the expectations of both doctors and patients. By measuring anatomical abnormalities, it may be a feasible approach to set normal appearance goals to achieve normal appearance outcomes. This article introduces the use of anthropometric assessment methods to accurately describe the anatomical abnormalities of hypospadias and proposes specific morphological goals for the reconstruction of various parts, implementing surgical operations in a goal-oriented manner. The aim is to establish a unified baseline decision-making system for hypospadias surgery, shorten the learning curve, improve the quality of clinical research, and achieve integrated reconstruction of structure, function, and aesthetics for patients.

The extracellular matrix (ECM) plays a pivotal role in regulating cellular behavior and driving tissue regeneration. Its unique structural characteristics and bioactivity not only provide physical support for cell growth, but also orchestrate tissue repair and functional reconstruction through multiple signaling pathways. This review systematically synthesizes preparation strategies for natural and engineered ECM materials from the perspective of ECM-mediated tissue regeneration mechanisms, with particular emphasis on recent advances in component preservation, structural biomimicry, and functional optimization. Furthermore, it delves into the application potential of cutting-edge technologies-including artificial intelligence, flexible electronics, and organoids-in ECM engineering, while critically analyzing the standardization and safety challenges hindering clinical translation. This article aims to provide a theoretical foundation and reference for constructing next-generation ECM-based regenerative medicine platforms.

Reconstructive surgery is fundamentally dedicated to restoring tissues and organs damaged by trauma, disease, or congenital anomalies, with the goal of re-establishing both physiological function and anatomical form. Facial reconstruction, as one of the most representative and technically demanding areas of the discipline, embodies the evolution of its concepts and technological progress. Using facial reconstruction as the point of departure, this article systematically delineates the scientific underpinnings and developmental frontiers of the field. Centered on four core elements-donor construction, vascular reconstruction, precision transplantation, and functional recovery, this article articulates the internal logic and technical considerations of both autologous and allogeneic reconstructive methods. Further, from the perspectives of regenerative donor fabrication, the digital and intelligent transformation of reconstructive surgery, breakthroughs in immune tolerance strategies, and the integration of engineering technologies to enhance functional outcomes, the article envisions potential paradigm shifts that may redefine the discipline. By leveraging facial reconstruction as a highly integrated lens, this work aims to elucidate the key drivers of innovation and chart the future directions of reconstructive surgery.

Objective: To review the research progress on lactylation modification in the pathogenesis of osteoarthritis (OA).

Methods: Relevant studies published in recent years on lactate metabolism and lactylation modification in OA were retrieved and analyzed, summarizing the molecular mechanisms of lactylation and its regulatory roles in different cells and pathological processes.

Results: Lactate, as the major metabolic product of glycolysis, not only participates in energy metabolism but also plays a crucial role in OA progression through lactylation modification. Lactate-driven histone and non-histone lactylation regulate gene transcription and cellular functions, contributing to chondrocyte metabolic reprogramming, extracellular matrix (ECM) synthesis and degradation, cell proliferation and apoptosis, as well as ferroptosis. In fibroblast-like synoviocytes, lactylation modification promotes cellular senescence and the release of inflammatory factors; in immune cells, lactylation regulates inflammatory responses by influencing macrophage polarization and intercellular communication. Overall, lactylation modification exhibits a dual effect in OA: it aggravates ECM degradation and inflammation on the one hand, but under specific microenvironments, it also promotes repair and regeneration. However, the site-specificity, cell-type heterogeneity, and cross-talk of lactylation with other epigenetic modifications remain to be further clarified.

Conclusion: Lactylation modification provides a novel perspective for understanding the metabolic and epigenetic mechanisms of OA and may serve as a potential biomarker and therapeutic target. Future studies combining multi-omics approaches to map the global lactylation landscape, together with small-molecule inhibitors, epigenetic editing tools, and regenerative medicine strategies, may enable precise regulation of lactylation, offering new strategies to delay or even reverse OA progression.