Sir, Professor Renton makes some very important and pertinent points in her letter published in the BDJ (Inadequate knowledge; BDJ 2012; 213: 197). The direct inferior alveolar nerve block (IANB) has been the corner stone of mandibular anaesthesia in dentistry for over 80 years but we do have a problem with it, as evidenced by the 63 patients with neuropathic injuries (NIs) resulting from IANB injections, seen on her clinic. The morbidity of prolonged anaesthesia or paraesthesia in the lingual nerve or inferior alveolar nerve has been highlighted by Professor Renton and it is sobering that over a dentist's working life, statistics suggest he or she may be responsible for 1-3 permanent NIs in their patients.

My feeling is that we need to look closely at the direct IANB and to see if we can minimise the risk of this injection leading to NI. Professor Renton mentions the increasing use of articaine as a buccal infiltration in the mandible for routine conservation or even extractions and the placement of implant fixtures. This technique obviates the need for an IANB altogether and so should be used wherever possible. There are two indirect approaches to anaesthetising the IAN, namely the Cow Gates injection and the Vazirini-Akinosi injection.1 These approaches have the great advantage that the injection is given some way away from the IAN and lingual nerve and so are much less likely to lead to NI. I think it is essential that every dental student graduating from a UK dental school should be proficient in giving these injections. They carry a high success rate but do take longer to take effect than the traditional direct approach.

Wherever possible, it is important not to give repeat, direct IANBs. A second injection can be responsible for further trauma and/or ischaemia to the lingual nerve or IAN and this might lead to a permanent NI. If it is felt that a second direct IANB has to be given, it is essential to use a brand new needle as the tip of a 27 gauge needle blunts the moment it penetrates the mucosa and so repeated use of the same needle could also lead to significant trauma to the tissues and the nerves.

The role of the vasoconstrictor in local anaesthesia should be investigated. For example, does ischaemia play a part in the causation of NI? Would it be better to use a plain local anaesthetic for a direct IANB rather than one containing a vasoconstrictor? Finally, I cannot understand why we continue to use 2.2 ml cartridges in the UK. Surely we should use the MINIMUM amount of a drug to achieve the desired effect and 1.7 ml or 1.8 ml is perfectly adequate. There is always a tendency for dentists to administer the entire contents of the local anaesthetic cartridge when giving an IANB. Reducing the amount of the drug by 23% might be helpful in reducing neurotoxic effects of the higher concentration local anaesthetic solutions.

There is no escaping the fact that permanent NI can occur as a result of a direct IANB injection and Professor Renton raises the point of warning patients about this potentially devastating complication. How can we do this in a potentially anxious patient with an acute irreversible pulpitis, where a high level of analgesia is required for root canal treatments? I think a discussion needs to be entered into on this topic with dentists, researchers, teachers, the defence organisations and our patients. Hopefully we can come up with a sensible protocol that warns patients but does not unduly frighten them.