## 1 Introduction  
Nerve lesions of iatrogenic origin can affect both sensory and motor trunks; these lesions can lead to potentially painful symptoms and dysfunctions of the oral and maxillofacial region [1; 2; 3]. In oral surgery, most of the lesions involve the sensory nerve trunks of the V cranial nerve, the inferior alveolar nerve, the lingual nerve, as well as the greater palatine nerve, albeit less frequently [1; 2; 3]. These lesions can be caused by a variety of treatments, such as oral or maxillofacial surgery, implant surgery, injection of local anesthetics, or endodontic treatments [1; 2; 3]. The neurological lesions can be divided into three degrees of increasing severity: neurapraxia, if the interruption is only functional and temporary of the nerve conduction; axonotness, if there is an anatomical interruption of the axons but with preservation of the sheaths covering the nerve, with functional recovery which happens if the regeneration takes place completely, but it is necessary for up to a few months. Finally, there is neurotness, characterized by the complete interruption of both the axons and the sheaths covering the nerve, where functional recovery of the nerve is rare [1; 2; 3]. Thus far, the approaches employed to reinstate the functionality of the impaired nerve have demonstrated challenges in achieving enduring outcomes [3; 4]. The currently accessible treatments are categorized as either surgical or non-surgical. Surgical methods encompass nerve transfer, nerve conduits, direct nerve repair, and the application of fibrin glue. Conversely, non-surgical therapies encompass pharmacological agents like analgesics, topical remedies such as corticosteroids, and the utilization of phytochemicals. It is necessary to underline that these therapies have disadvantages, as surgical therapies can have non-negligible adverse effects and require a specialized operator for execution, while non-surgical therapies have shown limited efficacy up to now [4]. Neurorrhaphy, the surgical repair of nerves, offers several alternative techniques to restore nerve function. These options include direct suturing (epineurial repair), which involves stitching the nerve ends together, maintaining nerve alignment. Cable grafting involves using a nerve graft or autograft to bridge a gap between nerve ends. Nerve connectors, such as tubes or stents, aid in nerve regeneration by facilitating the growth of nerve fibers across the gap. The use of nerve conduits, synthetic or biological tubes, guides nerve regrowth and prevents scar tissue formation. Nerve transfer involves rerouting a functional nerve to the injured area, allowing the restoration of lost functions. End-to-side neurornraphy involves connecting the injured nerve to a donor nerve's side, promoting axonal growth. Fibrin glue, platelet-rich plasma, and other bioactive substances can enhance nerve repair by promoting cell growth and angiogenesis. Minimally invasive techniques, like robotic-assisted neurornraphy, offer precision and reduced scarring. Combining different techniques, tailored to the patient's condition, can optimize nerve repair outcomes [4]. Among these methodologies, light-based therapy, known as photobiomodulation therapy (PBMT), has exhibited promising outcomes in various clinical and in vitro investigations [4]. Existing literature indicates that PBMT induces the migration and proliferation of clusters of neuronal fibers. In animal models of peripheral nerve compression injuries [5], PBMT has been shown to directly enhance the function of the damaged nerve, sustain nerve activity over time, and reduce or prevent scar tissue formation at the injury site [5; 6; 7]. Additionally, several researchers have observed that nerve injuries result in escalated oxygen consumption without a corresponding increase in ATP production. This phenomenon may arise from uncoupled respiration and energy production or a reversal of ATP synthetase activity, leading to ATP dissipation [5; 6].