The University of Sheffield
The School of Clinical Dentistry

Dr Simon Atkins, BDS (Sheff), MFDS RCS (Edin), PhD (Sheff), FDS RCS (Eng)

Unit of Oral and Maxillofacial Surgery and Oral Medicine
School of Clinical Dentistry
Claremont Crescent
Sheffield
S10 2TA
UK
Tel: +44 (0) 114 226 5462
Sec: +44 (0) 114 271 7849
Fax: +44 (0) 114 271 7863

Email: S.Atkins@sheffield.ac.uk

Biography

I am a Senior Clinical Lecturer and Consultant Oral Surgeon. My primary research and clinical interest is in the surgical management of trigeminal nerve injuries.

Research

My primary research interest relates the mechanisms surrounding regeneration following peripheral nerve repair, and the development of agents to improve recovery. I am a member of the Integrated Bioscience research group in the School of Clinical Dentistry, University of Sheffield and have a specialist interest in neuroscience.

Peripheral nerve injuries are common; it is estimated that there are 300,000 peripheral nerve injuries per year in Europe (1/1000 population). In 2007/8, 5,521 surgical nerve repairs were undertaken in England in the NHS. These injuries result in loss of sensory and/or motor function, and some patients develop chronic neuropathic pain. The management of nerve injury induced pain (dysaesthesia) is unsatisfactory and new therapeutic methods based on a better understanding of the aetiology are needed.

The role of inflammatory cytokines in the initiation of neuropathic pain after peripheral nerve repair This project investigates whether modification of the inflammatory cytokine profile at a site of peripheral nerve repair reduces ectopic neural discharge, and will hence reduce or prevent the development of neuropathic pain. This translational research will clarify the peripheral and central mechanisms underlying injury- induced neuropathic pain, and help identify potential therapeutic approaches.

The role of anti-scarring agents on regeneration following nerve trauma and repair. This translational research is investigating the effect of scar reducing agents on functional regeneration following peripheral nerve injury and repair with the aim of delivering a clinically effective agent.