Sir, oral cavity tumor excisions often leave a large defect requiring reconstructive surgery with a flap. The complications of these surgeries have three main origins – surgical procedure, general state of health and recipient site's quality – and may take different forms: infection, arterial/venous thrombosis, hematoma and dehiscence. Here the recipient site of the graft is also the oral cavity which is populated with a large number of bacteria, some of which are the main etiological factors of periodontal diseases. Ogihara et al.1 examined the benefits of antibiotic coverage in these surgeries. They conclude that an association of molecules targeting aerobes, anaerobes and Gram-negative bacteria has a greater action than that of a simple agent. This spectrum also covers periodontopathogenic bacteria. In their study, Kamizono et al.2 found 40% of post-operative site infection with a large number of Gram-negative anaerobic bacteria. Thus, periodontal disease could be a risk factor for flap failure by promoting the risk of local infection and managing the bacterial load of the recipient site seems to be paramount. However, it seems that periodontal disease can also have a role through inflammatory processes. This inflammation may have a local impact or a general impact. It can cause systemic inflammation by two main mechanisms: the local production of inflammation mediator within the periodontal tissues, thus increasing their overall rate and the release of pathogenic bacteria from periodontal tissues into the vascular system. The causal relationship between oral inflammation and the concentration of inflammatory compounds in the peripheral blood has been clearly demonstrated.3 Studies in animals have shown that periodontopathogenic bacteria may contribute to vascular inflammation by several mechanisms, such as the activation of Toll-like receptors, the increased production of pro-inflammatory mediators, and the expression of cell surface adhesion molecules. Similarly, Ohki et al.4 have shown that chronic periodontal disease has pro-thrombotic effects. However, free flap reconstruction requires vascular anastomosis and it is clearly established that low arterial quality is a risk factor for vascular anastomosis failure. Periodontal disease could thus act on two levels. Indeed, on the one hand it will induce an inflammatory syndrome that will promote the risk of failure through thrombosis, but on the other hand it will also increase the risk of infection through the periodontopathogenic bacteria which are present. Thus, periodontal decontamination may be indicated before this type of surgery.