Antibiotic bone cement accelerates diabetic foot wound healing—Elucidating the role of ROCK1 protein expression

We read with great interest the article titled 'Antibiotic bone cement accelerates diabetic foot wound healing: Elucidating the role of ROCK1 protein expression' by Yang C et al.1 This study revealed that antibiotic bone cement enhanced diabetic foot wound healing, possibly via upregulation of ROCK1. However, we found that there were few questions to be solved. Firstly, in the Results section, the authors applied vancomycin antibiotic bone cement to the wound after rigorous debridement in the experimental (EXP) group. They observed notable healing distally at the ankle joint, which facilitated limb preservation. The adaptation of the vancomycin bone cement technique demonstrated that antibiotic bone cement could offer a localized, sustained antibiotic release, mitigating infection risks and systemic antibiotic side effects while creating a conducive microenvironment for wound healing. However, based on the preoperative bacterial culture results, the Gram-negative bacteria, including proteus, pseudomonas aeruginosa, kleber pneumoniae and baumanii, accounted for 27.5% of the total number of cultured bacteria in the EXP group. Vancomycin is effective against most Gram-positive bacteria but has limited activity against Gram-negative bacteria, and is not typically used to treat infections caused by Gram-negative bacteria. We seek to understand whether the application of vancomycin bone cement in treating diabetic foot ulcers with these insensitive bacterial infections, as mentioned in the article, can also achieve the same ideal therapeutic effects. Based on our clinical treatment experience, using bone cement with other antibiotics that is sensitive to the bacteria could lead to better therapeutic outcomes. The efficacy of antimicrobial agents is crucial to the success of diabetic foot therapy. Secondly, the authors reported that diabetic foot cases with peripheral arterial disease constitute 70% of the cases in each group. Ischemia is the most critical factor impeding the healing of diabetic foot lesions.2 The assessment of the anatomical location, morphology and extent of vascular lesions facilitates decision-making regarding the treatment. Further diagnosis needs to be made based on the following parameters such as the ankle-brachial index (ABI) and toe-brachial index (TBI), transcutaneous oxygen pressure (TcPO2). The management of peripheral arterial disease encompasses antiplatelet therapy, vasoactive drug therapy and revascularization. The healing rate of foot ulcers notably increases after direct or indirect vascular reconstruction surgery.3 Brownrigg et al. reported lower limb revascularization could achieve a limb preservation rate of 80%–85% within 12 months and an ulcer healing rate >60%.4 To address our concerns, the article could clarify the treatment methods and outcomes for vascular lesions in the lower limbs of patients across each group. Different treatment methods may influence the final outcomes. In conclusion, addressing the aforementioned issues would undoubtedly enhance the overall quality of the article and broaden its appeal to readers. The authors declare no conflicts of interest. Data sharing is not applicable to this article as no new data were created or analysed in this study.