## 1 Introduction  
Post-traumatic trigeminal neuropathic pain (PTTNP) is a peripheral nerve injury that occurs following trauma to one or more branches of the trigeminal nerve, most commonly the inferior alveolar nerve (IAN) and the lingual nerve (LN) [1, 2]. Among the various etiologies, dental procedures--particularly implant placement, tooth extraction, and endodontic treatment--are frequently implicated due to the anatomical proximity of these nerves to the surgical sites in the posterior mandible [1, 2]. While dental implantology has achieved high technical success rates, the increasing number of procedures has led to a parallel rise in the reported cases of iatrogenic trigeminal nerve injuries, some of which progress to chronic neuropathic pain [3]. Pain is generally classified into three categories based on its underlying mechanisms: nociceptive, neuropathic, and neoplastic pain [4, 5, 6]. Nociceptive pain arises from the actual or potential damage to non-neural tissues and involves the activation of nociceptors, such as in trauma or inflammation [4; 5; 6]. Nociplastic pain, in contrast, results from altered nociceptive processing despite the absence of identifiable tissue or nerve injury and is commonly seen in functional pain syndromes such as fibromyalgia [4; 6; 4]. Neuropathic pain, the category under which PTTNP is classified, occurs as a direct consequence of a lesion or disease affecting the somatosensory nervous system [4; 5; 6]. The development of PTTNP involves complex pathophysiological mechanisms, including ectopic nerve firing, neuroma formation, peripheral and central sensitization, and maladaptive plasticity in the trigeminal system [7; 8]. These changes contribute to the persistent pain and sensory disturbances that extend beyond the expected period of tissue healing [7; 8]. PTTNP fulfills the diagnostic criteria for peripheral neuropathic pain, as it develops following trauma to the trigeminal nerve that causes a structural lesion and persistent sensory dysfunction [9; 10]. Affected patients frequently exhibit both negative sensory signs--such as hypoesthesia and anesthesia--and positive sensory phenomena--including dysesthesia, allodynia, and hyperalgesia [9; 10]. These symptoms are often chronic and significantly impair the patients' oral function, psychosocial well-being, and overall quality of life [11; 12]. Chronic orofacial neuropathic pain imposes a substantial burden on individuals and healthcare systems [13; 14]. Patients may experience difficulty in eating, speaking, and engaging in social activities, while long-term pharmacologic treatment or surgical interventions incur considerable costs and emotional distress [13; 14]. Several studies have identified the factors influencing the severity and prognosis of trigeminal nerve injury, including the trauma mechanism, the extent of the neural damage, and the timing of intervention [10; 11]. The Sunderland classification stratifies nerve injuries into five grades based on their structural severity, from a temporary conduction block (grade I) to a complete transection requiring surgical repair (grade V), with the prognosis worsening at a higher grade [15]. The timing of intervention is another critical determinant of recovery. From a neuropathic pain perspective, delayed treatment may lead to central sensitization and persistent ectopic nerve activity, which contribute to chronic pain that is less responsive to therapy. Early intervention within three months may interrupt this progression and improve outcomes [7; 8; 9; 16]. Clinical evidence strongly supports the value of early microsurgical repair [9; 16]. Studies have shown that patients undergoing surgical exploration and nerve repair within a few days to three months of injury exhibit significantly better outcomes than those receiving delayed treatment [9; 16]. Both [PERSON] et al. and [PERSON] et al.