Search

Patients suffering facial pain that does not fit with the traditional diagnostic criteria and which does not respond to dental treatment constitute a clinical problem. These patients lack a proper diagnosis and are frequently exposed to excessive and inadequate invasive treatment. The aim of this investigation was to study the long-term development of pain and the result of treatment in a cohort of patients suffering chronic idiopathic facial pain. The 74 patients referred to the Facial Pain Diagnostic Group at the Karolinska Institute School of Dentistry between 1981 and 1992 were invited to take part in a follow-up study. As 16 subjects were unwilling or unable to take part in the study and 13 had died, the remaining 45 were interviewed either in accordance with a standard protocol or by filling out a questionnaire mailed to them. The interview revealed that 10 were free of orofacial pain, but only 2 were totally free of pain. Over the 9-19 years' follow-up period the relationship between facial pain and pain in the rest of the body had changed substantially. Of 14 patients and more than 100 extractions, permanent pain relief was felt by only 3 patients. It is concluded that a diagnosis was given in only 2 cases. The distribution of the pain has changed dramatically. The low success rate of invasive treatments suggests that such therapeutic methods are to be considered contraindicated in patients suffering from idiopathic orofacial pain.

Although patients with chronic orofacial pain are frequently disabled, the disability is not necessarily due to the orofacial pain: various other factors may contribute. This retrospective study investigated the possible relationship between reports of pain, fatigue, disease conviction (DC), and denial of psychologic factors as explanation of the suffering (P-S) and limitations in occupational, domestic, physical, social, and sexual activities. The subjects comprised 30 patients referred to the Facial Pain Diagnostic Group at the Karolinska Institute, School of Dentistry, Huddinge, Sweden. None of the disability measures were significantly (p < or = 0.01) correlated with the facial pain reports. Fatigue was not correlated with degree of reported pain. DC was significantly (p < or = 0.01) correlated only with the minimum pain intensity. P-S was negatively correlated (p < or = 0.01) with maximum pain intensity and pain distribution (number of zones) outside the face. In 50% of the patients chronic orofacial pain was the formal reason for their occupational disability. However, such disability was related only to pain distribution (number of zones) outside the face. Social activity was negatively correlated (p < or = 0.01) with fatigue and positively correlated (p < or = 0.01) with P-S. It is suggested that the findings could be satisfactorily explained by a symptom perception hypothesis.

Patients with chronic orofacial pain often undergo endodontic therapy or surgery in an attempt to eliminate or relieve their symptoms. This study examined the relationship among invasive dental treatment, pain reports, and disease conviction in a group of patients referred for pain management. Forty-eight patients referred to the Facial Pain Diagnostic Group at the Karolinska Institute, School of Dentistry, Stockholm, were investigated retrospectively. There were 43 women and 5 men (age range, 30-81 years) with orofacial pain of more than 6 months' duration, which the patients considered to be of dental or paradental origin. Despite dental treatment intended to relieve the pain, no permanent relief had been achieved. There was no statistical correlation among the different pain reports, the individual types of treatment, and the disease conviction. The reason for the high degree of disease conviction in this type of patient warrants further investigation.

Chronic orofacial pain without obvious pathologic findings is not uncommon and is a diagnostic problem. It is uncertain whether this type of pain is different from other chronic idiopathic pain conditions. Fifty-five patients referred to the Facial Pain Diagnostic Group at The Karolinska Institute, School of Dentistry at Huddinge University Hospital, Stockholm, were investigated retrospectively. There were 49 women and 6 men, ranging in age from 30 to 81 years, all with orofacial pain of more than 6 months' duration, which the patients considered to be of dental or paradental origin. Despite dental treatment aimed to relieve the pain, no permanent relief was observed. The results suggest that chronic idiopathic orofacial pain resembles other chronic idiopathic pain, and adequate diagnosis and treatment require not only dental but also medical competence.

In order to study the effect of sodium acetylsalicylate and the role of prostaglandins on intradental nerve impulse activity experiments were performed on the teeth of anaesthetized cats. Nerve impulse activity was induced by mechanical and chemical stimuli and recorded by means of electrodes inserted into dentinal cavities. It was shown that such activity could not be blocked by sodium acetylsalicylate or indomethacin given locally or i.v. PGE2 failed to excite the sensory units when given locally (3.5 microng/ml) or intraarterially (35-140 ng/min) alone or in combination with mechanical and thermal stimuli or combined with local application of histamine (10 mg/ml) or bradykinin (10 mg/ml). Intraarterial infusion or arachidonic acid, a precursor to PGE2, PGF2 alpha PGG2 and PGH2 failed to change the excitability even on applying local stimuli to the pulp or with local application of histamine or bradykinin. These findings seem to indicate that the increased sensitivity of the tooth to thermal stimuli seen during acute pulpitis is not due to formation of prostaglandins.

In order to study the excitation of intradental nerves by fluid flow in dentinal tubules the following experiments were performed. The fluid flow was caused by reduced hydrostatic pressure applied to the exposed dentine surface of the canine teeth in the anesthetized cat. In one series of 7 cats the intradental nerve activity was recorded by means of electrodes inserted in dentinal cavities. Provided that the pressure was sufficiently reduced and applied to acid-etched dentine in preparations of sufficient depth, intradental nerve activity of different impulse amplitudes was recorded. The responding pressure sensitive units were found to be sensitized by a brief local application of veratrine and desensitized by potassium chloride. In the second series 26 single functional pulp nerve fibre units were dissected from the inferior alveolar nerve in 7 cats. Nerve impulses were recorded by means of platinum-iridium wire electrodes. The conduction velocities of the 9 fibres responding to reduced pressure varied from 8.3 to 43.0 m/s. Five of these fibres also responded to elevated pressure. None of the 9 fibres conducting impulses with a velocity below 2 m/s responded to a reduction in pressure. thus, the present data strongly suggest that intradental nerve endings with myelinated axons are activated by fluid flow in dentinal tubules. Our results support the hydrodynamic mechanism of dentine sensitivity.

In order to test the hypothesisthat ACh mediates the transmission of pain stimuli from dentin to sensory intradental nerve endings the following experiments were performed. Intradental nerve impulses were recorded by means of low impedance electrodes inserted in dentinal cavities in the tooth of the cat. An air blast proved to be an efficient physical stimulus to excite the intradental nerves. Local application of acetylcholine caused a similar response. This respinse to acetylcholine was followed by a transient blockage to repeated application. The response to acetylcholine could be blocked by d-tubocurarine, atropine, succinylcholine and hexamethonium administered locally. In contrast, the response to physical stimuli (air blasts) could not be blocked by these drugs. Moreover, during the period of depression following acetylcholine the preparation responded to physical stimuli. These findings suggest that acetllcholine is not a mediator in the intradental pain transmission provoked by physical stimuli.

The use of placebo in controlled clinical trials is a very difficult matter from an ethical point of view. Scientifically it offers probably the best way of obtaining fast and valid conclusions, thus promoting medical progress for the benefit of future patients. On the other hand, some patients may stand the risk of obtaining a suboptimal therapy in a placebo-controlled trial. In general, this latter aspect must be given precedence. Therefore the use of placebo control should be minimized and other control methods encouraged. However, in certain well-defined instances the use of a placebo control can be justified, provided the ethical implications can be handled.

Intradental nerve impulse activity can be recorded by means of electrodes inserted into dentinal cavities in the tooth of the cat. The following study has been conducted to investigate the origin ofthis impulse activity. The results suggest that the fibres from which the impulses are recorded must pass through the major part ofthe pulp between the recording electrodes. Furthermore, the results show that it is not possible to record discharges in the finest terminal branches in thepulpo-dentinal border zone using the present technique. However, the data obtained indicate that these terminal branches were activated during stimulation resulting in recordable propagated axonal impulses.

The hyperaemia produced by topical application of ketocaine-containing formulations was studied in human skin. The temperature in the hyperaemic area was unchanged or decreased which indicates that the hyperaemia was of a passive type, caused by a reduced flow in the venous side of the capillary bed.

A study in cats was designed to investigate the blocking of sensory nerve terminals by i.v. injection of lipid-soluble local anaesthetics such as lignocaine. I.v. injection of lignocaine 15--30 mg kg-1 did not completely block sensory nerve endings in the tooth of the cat, whilst tetrodotoxin (TTX) in large non-toxic doses did so. Based on the i.v. doses of TTX and the relationship between the local anaesthetic potency of the two substances when injected intra-arterially, it was calculated that lethal doses of i.v. administered lignocaine are necessary to block sensory nerve endings. It seems unlikely that peripheral pain pathways can be blocked by systemic i.v. injections of local anaesthetics.

Intradental sensory nerve impulse activity was recorded by means of electrodes inserted into dentinal cavities in the tooth of the cat. Impulses of different amplitudes was recorded. Local application of aconitine (10(-3) g/ml) and veratrine (10(-3) g/ml) induced nerve impulse activity. A rapid increase in the temperature of the tooth surface to 45-47 degrees C, which is known to induce fluid movements in the dentinal tubuli, did not induce any nerve impulse activity. However, after pretreatment of a tooth cavity with veratrine a rapid increase in the temperature of the tooth surface gave rise to nerve impulse activity. Steady state impulse activity induced by brief local application of aconitine was influenced by a rapid increase in the temperature of the tooth; during the increase in temperature impulses of low amplitude increased in frequency while impulses of high amplitude were blocked. Furthermore, reduced pressure applied to the exposed dentin, which also induces fluid movements in the dentin, gave rise to nerve impulse activity. Thus the sensory units in the tooth are stimulated by dentinal fluid movements and alkaloids known to excite mechanoreceptors increase their excitability. It is therefore suggested that the intradental sensory nerve endings are mechanosensitive structures.

The percutaneous penetration of the local anaestetic lidocaine was investigated in the guinea-pig. Three different types of composition were employed: lidocaine hydrochloride in aqueous solution, lidocaine base in an aqueous alcoholic solvent mixture and lidocaine base in aqueous solutions of dipolar aprotic solvents. The latter solvents included simple tertiary aliphatic amides, amides related to dimethylacetamide, some cyclic amides as well as a number of miscellaneous compounds. The degree of dermal anaesthesia was noted in each case. In addition, the uptake and distribution of lidocaine in the skin and its absorption into the blood were studied using tritium-labelled drug. The results show that the percutaneous penetration of lidocaine is dependent on the concentration of the agent, the time of epicutaneous application of the composition, whether the agent was used as salt or free base, and the nature of the solvent medium. Lidocaine base in aqueous dimethylacetamide was most effective in producing percutaneous local anaesthesia.

By means of experiments involving pin-pricking, compositions containing 10% ketocaine base in a mixture of 2-propanol, glycerol and water were found to produce a high frequency of block to cutaneous pain following application to volunteers under an occlusive dressing. The local analgesic efficacy was found to be directly related to the degree of saturation of ketocaine in the vehicle and time of application. The degree of hyperaemia observed in the treated skin areas was found to be related to the degree of local analgesia produced.