Pain transmission and central control mechanisms have evoked considerable interest in recent years. Extensive research has been and is being done into the subject, and the following three articles written by D. Bowsher, J. M. Mumford and F. T. Monks, who have had a long standing interest in this field, review the present concepts and cover, to some extent, the ideas of recent years that have led up to the present understanding of the subject. Dental pain, its production and the early part of its path o f transmission, is still a matter that is ill-understood. Both J. M. Mumford and F. T. Monks in their papers indicate this difficult problem from differing stand points. Is any part of the dentine innervated or not? Fearnhead and Lumsden (1956) and Fearnhead (1961) in their work on the innervation of teeth used a staining technique for nerve fibres on mature teeth. Their stain was based on silver nitrate which is notoriously capricious and must raise the problem of reliability. Monks (1951) used a silver protein compound, having first assessed its reliability, in a series of elegant histological investigations and came to the conclusion that nervous tissue was not present in the primitive pulp until after odontogenesis was firmly established and felt that under such circumstances it is unlikely for nervous tissue to be subsequently trapped in the advancing calcified dentine. Anderson (1976), in considering the transmission of stimuli across dentine regards the hydrodynamic theory of transmission as highly questionable considering the variable flow rates induced in dentinal tubules by a variety ofiso-osmotic solutions. Yet it is acknowledged that freshly cut dentine in the presence of a normal pulp is surprisingly insensitive. Sensitivity of dentine appears to be associated with pulpal oedema, yet it has not been emphasised that as the pulp is enclosed in a rigid box, and when under pressure, as in situations of oedema, it is likely that although a minimal fl0w of fluid in a tubule will produce a small stimulus at a receptor, the threshold level may be so lowered, it will result in the excitation of the afferent nerve. The fact that different iso-osmotic solutions give different flow rates in dentinal tubules would appear to be irrelevant in conditions of oedema but may be significant for their variable effect on the normal pulp. Speed of conduction across dentine is impressive clinically. Mechanical stimulation would produce a pressure wave in the tubules (rigid walled tubes) travelling at a speed of about 17 metres per second (Bradley, 1976) which is approximately the speed of conduction in a C pain fibre. Even if nervous tissue did penetrate the dentine to some extent, as Mumford suggests, the relationship of the odontoblast and its process with the nervous system is still not known. Would it be too far fetched to consider that the odontoblast and its process is a mechano-receptor and the afferent nerves merely synapse with the surface of the odontoblast in the predentine layer ? Or is the process a pressure effect in the pulp mediated by the liberation of a histamine-like substance as Monks suggests in his article. Recent work by Kollar and Lumsden (1979) suggests very early innervation of the pulp, contrary to Monks (l 951) findings who did demonstrate, however, early innervation of the follicle and sub-epithelial layer. The answers to many of these questions are still awaited, but reading these articles makes one feel that we are a little nearer the truth than we were: teeth are peculiar structures anatomically, embryologically and to some extent, physiologically.