Professor Peter P Robinson ( BDS, FDSRCS, PhD, DSc, F.Med.Sci )

Professor of Oral and Maxillofacial Surgery

Tel: 0114 271 7964
Fax: 0114 271 7863

Administrative roles in School/Department

Oral Neuroscience Research Group Leader

National administrative roles

President of the Association of British Academic Oral and Maxillofacial Surgeons

Research Interests

The research of our group has answered a series of fundamental neuroscience questions about the effects of trigeminal nerve injuries and, by using the principles derived in the laboratory to guide clinical decisions, has led to improved patient care. In order to achieve this we have pursued a wide range of activities, from basic science studies undertaken within the field of oral biology, through to clinical investigations on patients. We have laboratories dedicated to electrophysiological and immunocytochemical studies, and run a clinical service for the treatment of patients with nerve injuries.

Trigeminal nerve injuries are common and can be extremely distressing for the patient. The inferior alveolar and lingual nerves are most frequently damaged during lower third molar removal, but may also suffer injury during orthognathic surgery or as a result of facial fractures. Although most patients regain normal sensation within a few weeks or months, a proportion are left with paraesthesia or dysaesthesia which can cause difficulty with speech and mastication, and are a frequent cause of litigation against the surgeon. Little was offered to these patients, either in terms of a clear prognosis or possible surgical intervention to improve the level of recovery. Now, as a result of our work, it is possible to answer a number of fundamental questions, such as:

Should we intervene surgically, and how?
Yes we should intervene in some circumstances, as nerve repair can improve recovery. Detailed analysis of functionally distinct nerve fibre groups reveals that repair of a cut lingual nerve using epineurial sutures is more effective than entubulation and, if a damaged nerve segment has to be excised, repair by stretching the ends under slight tension is better than grafting. Delay prior to lingual nerve repair is essential as, in the early stages after injury, it is not possible to distinguish between anaesthesia resulting from a crush injury (which will not require intervention) and that resulting from a section injury (which requires repair). This distinction can normally be made at approximately three months post-injury and, fortunately, our studies have shown that this delay has little effect on the outcome.
These principles of lingual nerve injury management have been applied to a series of patients referred from throughout the UK and abroad. Our prospective, quantitative assessment of the outcome of lingual nerve repair, using the first scientifically-based protocol, is the largest published single-centre series in the world literature. It has revealed that, although the outcome is variable, there is a highly significant improvement in the majority, and patients consider the surgery worthwhile.

Can we enhance regeneration?
Electrophysiological studies have shown that incorporation of nerve growth factor at a site of lingual nerve repair preferentially enhances the regeneration of thermosensitive afferents, suggesting that it may play a role in determining the phenotypic profile of the regenerating axonal population. This suggests that future therapeutic enhancement of regeneration after peripheral nerve injury may require a combination of factors to encourage regeneration of specific fibre groups. A very recent study has shown an inverse correlation between the level of recovery and the extent of scar formation at a site of nerve repair. We are therefore currently investigating the effect of scar reducing agents, as these may permit enhanced regeneration.

How can injuries be prevented?
The most important approach to nerve injuries is prevention. The incidence of lingual nerve injuries during third molar surgery in the UK is significantly higher than in other parts of Europe and in the USA. We have shown that this difference results from the UK method of elevation of a lingual flap and insertion of a Howarth´s periosteal elevator. We undertook the first randomised controlled trial into the effect of this surgical technique, and found that avoidance of lingual flap retraction resulted in a significant reduction in lingual nerve injury. We concluded that, for the majority of cases, lingual retraction should be avoided. This has led to an evidence-based change in the recommended surgical technique taught in the UK, and has had a substantial impact on clinical practice.

How can we reduce injury-induced pain?
At present, little can be offered to patients who suffer from the persistent painful condition of dysaesthesia, and understanding the aetiology of this disorder remains one of our key objectives. We have shown that if a nerve is constricted, sectioned or tightly ligated, neuropeptides accumulate at the injury site and some damaged axons become spontaneously active and mechanically sensitive. As the time course of the abnormal activity and neuropeptide accumulation is very similar, we believe that they may be linked, and that this could provide a pharmacological approach to treatment. We are studying neuropeptide accumulation and other changes in a unique archive of human lingual nerve tissue (obtained at the time of repair) in order to assess direct correlations with symptomatology. Ultrastructural sudies on this tissue have shown that both myelinated and unmyelinated fibres are smaller than normal and the unmyelinated fibres show a significantly higher incidence of both axonal exposure and axonal apposition. These ultrastructural changes may account for some of the altered electrophysiological characteristics. In other studies we have shown changes in expression of other regulators of neuronal excitability, such as nitric oxide and specific sodium channel subtypes. In pharmacological studies we have found that the application of corticosteroids to an injury site decreases the mechanically-induced ectopic discharge, and carbamazepine reduces the spontaneous discharge in some axons. We are undertaking clinical trials on the use of potential agents.

In summary, these investigations have provided a clearer understanding of the sequelae of trigeminal nerve injuries, how they might best be treated, and how some of them may be avoided.

Recently published papers

Current management of damage to the inferior alveolar and lingual nerves as a result of removal of third molars. British Journal of Oral & Maxillofacial Surgery, 42; 285-292, 2004.

Peripheral mechanisms for the initiation of pain following trigeminal nerve injuries. P P Robinson, F M Boissonade, A R Loescher, K G Smith, J M Yates, et al J Orofacial Pain, 18; 287-292, 2004.

Close apposition and exposure of non-myelinated axons in traumatic neuromas of the human lingual nerve. A R Vora, A R Loescher, F M Boissonade & P P Robinson. J Peripheral Nervous System, 9; 200-208, 2004.

Ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve. A R Vora, A R Loescher, F M Boissonade & P P Robinson. J Orofacial Pain, 19; 22-33, 2005.

Nav1.7 sodium channel expression in human lingual nerve neuromas. E V Bird, F M Boissonade, P P Robinson. Archives of Oral Biology, 2006.

Inflammatory cell accumulation in traumatic neuromas of the human lingual nerve. A R Vora, S Bodell, K G Smith, A R Loescher, P P Robinson & F M Boissonade . Archives of Oral Biology, 2006.

Vanilloid receptor 1 (TRPV1) expression in human lingual nerve neuromas from patients with or without symptoms of burning pain. J E Biggs, J M Yates, A R Loescher, N M Clayton, F M Boissonade, P P Robinson. Brain Research, 2006.

Current MPhil / PhD students

Simon Atkins – The effect of scarring on axonal regeneration after peripheral nerve injury. (co-supervised with K G Smith, A R Loescher & F M Boissonade).

James Biggs – The role of TRPV1 and P2X3 in trigeminal neuropathic pain. (co-supervised with J M Yates, A R Loescher & F M Boissonade).

Yvonne Fok – The role of uninjured neurones in trigeminal nerve injury-induced pain. (co-supervised with D Andrew, M Worsley & F M Boissonade).

Mark Barber – The role of thermosensitive transient receptor potential channels in human dental pain. (co-supervised with H D Rodd & F M Boissonade).