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M V Närhi

Publications and source records attributed to M V Närhi.

14 recordsLinked to original sources
PubMed1999

Dental injury models: experimental tools for understanding neuroinflammatory interactions and polymodal nociceptor functions.

Recent research has shown that peripheral mechanisms of pain are much more complex than previously thought, and they differ for acutely injured normal tissues compared with chronic inflammation or neuropathic (nerve injury) pain. The purpose of the present review is to describe uses of dental injury models as experimental tools for understanding the normal functions of polymodal nociceptive nerves in healthy tissues, their neuroinflammatory interactions, and their roles in healing. A brief review of normal dental innervation and its interactions with healthy pulp tissue will be presented first, as a framework for understanding the changes that occur after injury. Then, the different types of dental injury that allow gradation of the extent of tissue damage will be described, along with the degree and duration of inflammation, the types of reactions in the trigeminal ganglion and brainstem, and the type of healing. The dental injury models have some unique features compared with neuroinflammation paradigms that affect other peripheral tissues such as skin, viscera, and joints. Peripheral inflammation models can all be contrasted to nerve injury studies that produce a different kind of neuroplasticity and neuropathic pain. Each of these models provides different insights about the normal and pathologic functions of peripheral nerve fibers and their effects on tissue homeostasis, inflammation, and wound healing. The physical confinement of dental pulp and its innervation within the tooth, the high incidence of polymodal A-delta and C-fibers in pulp and dentin, and the somatotopic organization of the trigeminal ganglion provide some special advantages for experimental design when dental injury models are used for the study of neuroinflammatory interactions.

Animals↗
PubMed1988

Acute and chronic reactions of dental sensory nerve fibers to cavities and desiccation in rat molars.

We have studied the effects of air drying of exposed, acid etched dentin on the sensory innervation of rat molars. In the acute series of experiments, trigeminal nerve fibers were labeled by axonal transport of radioactive protein prior to the dentin exposure and desiccation, the anesthetized rats were fixed by aldehyde perfusion 10 min later, and the teeth were prepared for autoradiography. The results confirmed the hydrodynamic theory by showing outward movement of labeled nerve material in response to dentinal drilling and desiccation. It also showed that some odontoblasts could be separated from the dentinal nerve fibers. In the chronic series, teeth were injured 25 h, 5-7 days, or 21 days prior to fixation and nerves were labeled during the last 24 hours; the surviving vital nerve fibers were evident because of their axonal transport of the radioactive label. In that series, sensory nerve fibers were found to have been lost from areas with newly-formed reparative dentin, or from dentinal tubules that had lost their odontoblasts. In the teeth injured 25 h, 5-7 days, or 21 days earlier, an abnormal nonneuronal labeling occurred 0.2-0.3 mm into injured dentin. Our results are discussed in relation to the hydrodynamic theory, nerve-odontoblast interactions, differences between shallow and deep cavity injuries, altered nerve location in response to pulpal or dentinal injury, and characteristics of the pulp-dentin border.

Animals↗
PubMed1987

Sensory innervation of pulp and dentin in adult dog teeth as demonstrated by autoradiography.

In order to study the location of sensory nerve fibers in dog teeth, we injected 3H-amino acids into the left trigeminal ganglion of 2 anesthetized adult dogs; we then waited 24 hours for axonal transport of labeled protein and prepared the fixed decalcified teeth for autoradiography. Heavily labeled sensory neurons were found in the maxillary and mandibular divisions of each injected ganglion and its peripheral nerves and central root. Numerous labeled axons were found entering dental roots; they arborized mostly in the crown to end in peripheral pulp or inner dentin. Some labeled fibers extended 150-175 microns into dentinal tubules, but most intradentinally labeled fibers were less than 100 microns long. The dentinal innervation was most concentrated in the crown, with autoradiographic label over more than 50% of the tubules at the tip of each pulp horn. Differences in innervation density for coronal, cervical, intercuspal, septal, radicular, and reparative dentin were analyzed. In some regions, labeled endings branched along the pulp-predentin border but did not enter the dentinal tubules. Electron microscopic autoradiograms were prepared to confirm specific labeling of nerve fibers and nerve endings, and to describe their ultrastructure and association with odontoblasts. The results show that labeled sensory fibers in dog teeth have an ultrastructure similar to that described previously for rat molars and for monkey and cat teeth. No specific junctions were found between labeled sensory fibers and odontoblasts, in agreement with previous studies of other teeth.

Animals↗
PubMed1987

The response of dog intradental nerves to hypertonic solutions of CaCl2 and NaCl, and other stimuli, applied to exposed dentine.

Responses of single nerve units from the canine and incisor pulps of anaesthetized beagles to CaCl2 (3.5 M, 4.9 M and saturated) and NaCl (2.5 M and 4.0 M) were recorded. The sensitivity of these nerve units to drilling and probing of dentine, and to drying with air blasts, was also studied. Twenty-one out of 22 units responded immediately, either with a few spikes or, sometimes, with a 2-5 s train of impulses, to hypertonic CaCl2 when applied to superficial dentine. Deep in dentine, CaCl2 induced immediately responses in 15 out of 21 units. There were responses to hypertonic NaCl in 15 out of 19 units, but only when applied deep in dentine. This firing had a latency of 15-300 s (mean 94 s) and continued until the solution was washed away. Units sensitive to CaCl2 also responded to drilling, probing and drying. When applied to the exposed pulp, CaCl2 never induced nerve activity, but hypertonic NaCl induced responses in all units tested (n = 19); the latencies were 0-300 s (mean 34 s). The mechanism of nerve activation in response to hypertonic CaCl2 is probably hydrodynamic, and common to several other stimuli as in drilling, probing and air drying. Responses to hypertonic NaCl may have been induced by a direct excitatory effect of Na+-ions on the nerve endings or axons in the pulp-dentine border.

Animals↗
PubMed1986

The effect of dentinal stimulation on pulp nerve function and pulp morphology in the dog.

The effect of dentinal stimulation on pulpal nerve responses and pulp morphology has been studied in the dog. Canine tooth (n = 25) dentin was stimulated by drilling, probing, and air-blasting for from two to five hours. Acid-etching was used to open dentinal tubules. All test teeth showed disruption of the odontoblast layer and its separation from the predentin; also, dislocation of odontoblast nuclei into dentinal tubules was found in most cases. Single-fiber (n = 14, conduction velocity = 24.3 +/- 7.4 (SD) m/s) recordings of the responses of canine tooth pulpal nerves to dentinal stimulation were made in ten of the stimulated teeth. No changes in the sensitivity of the nerves to dentinal stimulation could be detected. It is concluded that pulpal nerve function and morphological changes of the pulp are not clearly correlated. The condition of the dentin surface seems to be the important factor.

Acid Etching, Dental↗
PubMed1982

Activation of intradental nerves in the dog to some stimuli applied to the dentine.

Both scraping of superficial dentine and air blasts induced bursts of action potentials in 19 out of 22 units immediately. In 5 out of 16 units 4.9 mol/l CaCl2-solution was also effective. Dry absorbent cotton activated 5 out of 16 units with a 10-20 s latency. All 18 units tested responded to mechanical irritation of the pulp. Acid etching of dentine made the units more sensitive. Resin impregnation abolished the responses. Drilling of dentine with a turbine bur induced responses of the same type as air blasts. Three units responded to heat and 2 also to cold. Hypertonic NaCl-solution was only effective when applied either to the pulp (in 9 out of 12 units) or to the inner dentine (in 5 out of 17 units). It is concluded that intradental nerve fibres sensitive to several different stimuli exist in the dog. Many of the stimuli used induce fluid flow in dentinal tubules in vitro. Nerve activation might have been due to the same mechanism with all stimuli used, possibly to mechanical distortion of the peripheral pulp tissue as a result of the fluid flow. The findings support the hydrodynamic hypothesis of dentine sensitivity.

Action Potentials↗
PubMed1982

Responses of intradental nerve fibres to stimulation of dentine and pulp.

In the present work responses of intradental nerve fibres to stimuli that induce fluid flow in dentinal tubules as well as to direct mechanical irritation of the exposed pulp were studied on 9 young adult beagle dogs. Under pentobarbitone anesthesia 31 single functional intradental fibre units were dissected from the mandibular nerve. Stimuli were applied to the lower left canine tooth. Exposed dentine surface was irritated by scraping, air blasts and dry absorbent paper and the pulp mechanically with a von Frey hair. Ten fibre units responded to stimulation of dentine. Six of them were also tested with mechanical irritation of the pulp and were all responsive. Fifteen of twenty fibres responded to mechanical stimulation of the pulp. The mechanosensitive nerve fibres were all A-type according to conduction velocities (mean 25.6 +/- 8.1 (SD) m/s). It is concluded that there exist mechanosensitive intradental A-nerve fibres in the dog which are activated by stimuli that induce fluid flow in dentinal tubules. Nerve fibres of this type could be responsible for dentine sensitivity in man. Consequently, the present study gives support to the hydrodynamic hypothesis of dentine sensitivity. Moreover, mechanosensitive nerve fibres could also be responsible for the pain symptoms of pulpal inflammation, because pulpitis may also create suitable circumstances for their activation.

Animals↗
PubMed1980

Distension of pulmonary vein--left atrial junction: heart rate responses in conscious and anesthetized dogs.

The cardiac chronotropic effects of distension of pulmonary vein-left atrial junction were investigated in conscious dogs and in dogs anesthetized with intravenous alpha-chloralose (100 mg/kg) or pentobarbital (30 mg/kg). All the experiments were made on trained, chronically instrumented, closed chest animals held in horizontal position. Inflation of a single small balloon in the junction elicited a tachycardic response both in conscious and chloralose-anesthetized dogs, while in pentobarbital anesthesia no change in heart rate was found. Contrary to reports of other investigators, no transient bradycardia was found, nor any correlation between predistension heart rate and the increase in heart rate due to the distension. It is suggested that the choice of anesthetic can be done only after its modifying effect on the parameter studied is known. Only the use of trained, chronically instrumented and conscious dogs will reveal this effect.

Animals↗