Tema: Smerte og smertelindring
Matti Närhi, Lars Bjørndal, Maria Pigg, Inge Fristadand Sivakami Rethnam Haug
The present article, a review aiming to update the readeron current knowledge on pulpal and dentinal pain, is the first ina series of articles on the theme "Pain and pain management".
The specialized anatomy of the pulp-dentin complex and the dense,predominantly nociceptive pulpal innervation from the trigeminalnerve explain the variety of pain sensations from this organ.
Brief, sharp pain is typical of A-fiber-mediated pain, while long-lasting,dull/aching pain indicates C-fiber involvement. A-fibers react tocold or mechanical stimuli, such as cold drinks or toothbrushing,while C-fibers are mainly activated by inflammatory mediators. Thus,lingering pain suggests presence of irreversible pulpal inflammation.
During pulpitis, structural changes of the pulpal nerves (sprouting)occur and neuropeptide release triggers an immune response; neurogenicinflammation. Pain sensations during pulpitis can range from hypersensitivityto thermal stimuli to severe throbbing, aching pain that can bereferred and often difficult to localize making diagnosis a challengingsituation for the clinician.
Surface biofilm amplifies hypersensitivity of exposed dentin surfacesbecause irritants reach the pulp through open dentin tubules, producinginflammation. Removing the biofilm reduces dentin hypersensitivitybut supplemental treatment aiming to reduce dentin permeability,is often necessary. Caries removal and filling therapy is adequateduring reversible pulpitis if the pulp has maintained its abilityto distance itself from the bacterial assault by producing reparativedentin. However, endodontic therapy is necessary when pulpitis hasreached an irreversible stage.
Pain localized to teeth is among the most frequently experienced orofacialpain complaints, with a prevalence of 12 % in the general populationwithin a 6-month period (1). Tooth pain may be attributed to a varietyof conditions, which may be acute or chronic in nature, local orsystemic in origin, but is most frequently an indication of damageor disease in the tooth or its surrounding tissues. A good understandingof structures and mechanisms underlying the painful sensation isa prerequisite to pain management.
Innervation of the dental pulp and dentin
The dental pulp resides in a rigid capsule consisting of dentinand enamel. This creates a low-compliant environment that makesthe pulp tissue unique (2, 3). The dental pulp is richly innervatedmainly by axons from the trigeminal nerve, predominantly sensoryin nature and mainly committed to pain perception (nociception).A smaller population of pulpal nerves are autonomic sympatheticfibers emanating from the superior cervical ganglion and associated withpulpal vasoconstriction (4).
Extremely strong pain - reaching the maximum intensity at any painscore - can be induced by activation of intradental nerves (5 -7). Such intense pain responses can be explained by the dense (Figures1 and 2) and predominantly nociceptive innervation of the pulp anddentin (6, 8). The transmission of the pain-inducing stimuli throughdentin from its exposed surface is exceptionally effective and allowseven very light stimuli, such as air blast and probing, to be intensifiedin a way that may induce tissue injury and subsequent nerve activationat the pulp-dentin border (5). Each tooth is innervated by abouta thousand trigeminal axons (9 - 11), which may have branched beforeentering the apical foramen and may innervate more than one tooth.In the radicular pulp, the nerve fibers are bundled together, butonce they reach the coronal pulp (8, 12, 13), they divide into smallerbundles. The axons then branch extensively and each may form 50- 100 terminals in the peripheral pulp, forming a network underthe odontoblast layer, known as the plexus of Raschkow. The densityof nerve endings is especially high in the pulp horns, where asmany as 50 % of the dentinal tubules are innervated. Many of thetubules contain multiple nerve terminals (8). There are approximately20 000 - 30 000 nociceptive nerve endings/mm2 in the pulp-dentinborder area in the most coronal pulp which accounts for the extremelyhigh sensitivity of dentin.
Nerve fiber types: A- and C-fibers, their functionaldifferences
There are both myelinated (20 - 25 %) and unmyelinated (75 -80 %) afferent nerve fibers in the pulp (8, 12, 13). These two fibergroups differ greatly in their functional properties (6, 7, 14,15). The myelinated fibers belong predominantly to the Ad- but apart of them to Ab-group and are fast conducting (from 3 up to 50- 60 m/s (6, 7, 14, 15). The A-fiber endings are located in theperipheral pulp and inner dentin (Figs. 1, 2 and Table 1). Theyare responsible for dentin sensitivity, and their activation inhealthy teeth results in sharp and usually short-lasting pain, notoutlasting the stimulus (5 - 7, 16).
There are also a number of larger Ad-fibers (approximately 10% that enter the pulp at the apex). These are not active in thehealthy pulp but become active when inflammation is present. Thisis an example of `peripheral sensitization' when normally non-noxious nervefibers are recruited to the pain system. All the sensory nerve fibersthat enter the pulp branch and get narrower as they travel to thepulp cornua. Four times as many nerve fibers can be counted at themid-crown level of the pulp than at the apical level. Myelinated nervefibers commonly have non-myelinated terminals, making it difficultto differentiate the terminals of fast and slow fibers (13, 17).
The non-myelinated nerves are C-fibers having slow conduction velocities(0.5 - 2.5 m/s) and their terminals are located in the pulp proper.They are predominately sensory with a small population of sympathetics(10 %). The majority (70 %) of the axons entering the apex are C-fibers.
From the clinical point ofview it is important to note that the sharp, short lasting, non-lingering,pain due to stimulation of exposed dentin can be evoked when thepulp is healthy or has some minor reversible injury and, thus, can successfullybe managed without root canal treatment.
The C-fibers are polymodal and respond to several different noxiousstimuli. In other sites they are activated by intense heat and coldand many inflammatory mediators such as histamine and bradykinin(7). In the pulp they are activated during inflammation, and increasinglyso in its advanced stages (7). It seems that they may conduct thedull pain or ache in pulpal inflammation (5, 7).
Considering the responsecharacteristics of the C-fibers it can be concluded that their activation,inducing dull aching pain, which is often long-lasting or lingeringin nature, may suggest that the pulp is irreversibly damaged andmight need root canal treatment.
In addition, nerve fibers release biologically active peptides, knownas neuropeptides, which influence neural activity and functioning(18). Neuropeptides in the dental pulp are released from the nerveterminals of mainly A?- and C-fibers. There are numerous neuropeptidesin the dental pulp which are commonly classified as sensory, sympatheticor parasympathetic according to the origin of nerve fibers. Sensoryand sympathetic neuropeptides are synthesized in the trigeminaland superior cervical ganglion, respectively (19).
Sensory neuropeptides are e.g. calcitonin gene-related peptide (CGRP),substance P (SP) and neurokinin A. Neuropeptide Y (NPY) is co-releasedwith noradrenaline from the sympathetic nerve terminals. The mostabundant neuropeptide in the dental pulp is CGRP, followed by SP.CGRP is a vasodilator while SP increases capillary permeability.NPY is a vasoconstrictor and modulates the immune function (20).When injected in the blood stream in experimental studies, CGRP,SP and NKA produce vasodilation (21), whereas activation of pulpalnerves by electrical stimulation produces long-lasting vasodilationin the pulp due to release of CGRP (22 - 24).
Changes in the nerve function in inflammation,neurogenic inflammation, inflammatory mediators
Structural changes of nerve fibers occur in response to inflammation.Nerve fibers sprout or branch extensively (25, 26), thereby increasingthe release of neuropeptides resulting in "neurogenic inflammation".CGRP and SP are increased at initial stages of pulpal inflammation,whereas NPY increases in chronic stages (27). Neuropeptides releasedfrom sensory neurons not only act on the vasculature, but also directlyattract and activate innate immune cells (dendritic cells) and adaptiveimmune cells (T lymphocytes) (28, 29). Once immune cells are recruitedto the site of inflammation, inflammatory mediators such as cytokines,histamine, bradykinin, prostaglandins, leukotrienes, and numerousother substances are released. Neural sprouting increases neuropeptidecontent and release, resulting in neurogenic inflammation (30, 31).Figure 3 schematically illustrates the 5 stages of changes to thedentin-pulp complex according to caries progression, possible symptomsand suggested treatment. Caries, even limited to the enamel layermay already have some minor effect on the dental pulp (5), e.g.in terms of neurogenic inflammation and onset of dentin sclerosiscan occur, that corresponds with alteration along the odontoblastlayer (32) (Stage 1). Sprouting of sensory neuropeptide containingnerve fibers occurs with deeper carious lesions (Stage 2 and 3)coinciding with hyper- and thermal sensitivity of a tooth (26, 31,33). This sprouting is reversible and subsides to normal after cariesarrestment or restoration. Irritation of the dental pulp due tocaries leads to reparative dentin formation by odontoblasts. Withthe progression of caries (stage 4), localized microabscesses mayform in the dental pulp with sprouting of nerve fibers. There isalso increased release of neuropeptides (34).
Increased release of sensory neuropeptidesin the dental pulp causes vasodilation, leading to increased localtissue pressure and increased capillary permeability, causing plasmaextravasation and edema formation. Due to the non-compliant natureof the dental pulp, clinically this can be felt as throbbing pain.
As the contaminated demineralized carious dentin reaches the dentalpulp (stage 5), pulpal inflammation becomes extensive with partialnecrosis combined with reparative dentin formation and vital inflamedpulp apically. Due to the loss of functional barrier against infectionand limited capacity for healing in the coronal portion of pulpat this stage, necrosis progresses apically. Symptoms can be numerousand variable at this stage and when left untreated, infection andinflammation progresses, eventually leading to complete pulpal necrosisand apical periodontitis.
Mechanism of nerve activation in response to dentinal stimulation,dentin sensitivity
How stimuli are relayed from the peripheral dentin to the sensory terminalslocated in the region of the dentin-pulp border zone has been asubject of interest for many years. Evidence indicates that movementof fluid in the dentinal tubules is a crucial factor in dentinalpain. Pain-producing stimuli, such as heat, cold, air blasts, andprobing with the tip of an explorer, have the ability to displace fluidin the tubules (35, 36). This is referred to as the hydrodynamic mechanismof dentin sensitivity.
The hydrodynamic theory suggests that dentinal pain associated withstimulation of a sensitive tooth ultimately involves mechanotransduction.Recently, classical mechanotransducers have been recognized on pulpalafferents, providing a mechanistic support to this theory (37).Thus, fluid movement in the dentinal tubules is translated intoelectric signals by activation of mechanosensitive ion channelslocated in the axon terminals. Using single-fiber recording techniques,a positive correlation was found between the degree of pressurechange and the number of nerve impulses leaving the pulp (38 - 40).The outward fluid movement (negative pressure) produces a much strongernerve response than inward movements (36, 40).
A short application of cold or heat to the outer surface of dentin canevoke pain that is not dependent on temperature changes in the pulp(38, 41). The response to thermal stimulation is rapid, although thethermal conductivity of dentin is relatively low. Heat expands thefluid within the tubules, causing the fluid to flow towards the pulp,whereas cold causes the fluid to contract, producing an outwardflow.
It is principally the A-fibers that are activated by a rapiddisplacement of the tubular contents (Table 1 and Figure 1) (42).C-fibers, however, may be activated by heat (above 43° C). The polymodal C-fibernociceptors contain numerous receptors which respond to differenttypes of stimuli (43, 44). Particularly, a receptor termed the "transientreceptor potential, subtype vanilloid 1" or TRPV1 is expressed,and responds to heat above 43° C, certain inflammatory mediators,and acid (pH <6) (45). Eugenol activates and ultimately desensitizesTRPV1, and this may explain the anodyne action of zinc oxide eugenoltemporary restorations (46).
It has also been shown that pain-producing stimuli are more readilytransmitted from the dentin surface when the exposed tubule aperturesare open and the fluid within the tubules is free to flow outward.For example, acid treatment of exposed dentin to remove the smearlayer opens the tubule orifices and makes the dentin much more responsiveto stimuli such as air blasts and probing.
The hydrodynamic theory is also applicable to explain hypersensitivedentin. It has been questioned whether exposed dentin is simplysensitive or becomes truly hypersensitive. However, evidence indicatesthat new sodium channels, capable of activating nerves, are expressedin nerve tissue exposed to inflammation. An increase in the densityof sodium channels or their sensitivity may therefor contributeto dentinal hypersensitivity. Hypersensitivity typically occursin the cervical area where the dentin is exposed because the protectiveenamel/cement was not formed or is worn out or etched away (Figs.4 and 5). The odontoblasts and/or pulp cells respond by formingintratubular deposits or eventually tertiary dentin is laid down.This results in narrowing or closing of the dentinal tubuli. Depositionof tertiary dentin leads to decreased conductivity compared to theprimary and secondary dentin. In addition, deposition of tertiarydentin without involvement of primary odontoblast cells over thepulpal ends of the exposed tubules may also reduce the sensitivity,as reparative dentin is less innervated by sensory nerve fibers.Some hypersensitive dentin, however, does not spontaneously desensitize,indicating either an ongoing inflammatory change or mechanical changesin the patency of dentinal tubules.
Dentin hypersensitivity, development, preventionand treatment
The prevalence of individuals claiming to have dentin hypersensitivityhas been reported to between 3 - 57 % and most frequently in patientsbetween 20 and 40 years (47).
Bacteria and dentin hypersensitivity
A wear facet or non-carious cervical lesion may be very painful, andconsequently the patient may avoid daily use of this particular toothand oral hygiene procedures. This may in turn develop into evenmore severe pain. In cases where a biofilm develops, the bacteriaand their metabolites penetrate the dentin, resulting in local inflammatorychanges in the pulp, including neurogenic inflammation as describedabove. Due to the pain, the person may tend to leave the site undisturbed.This may have two clinical effects; firstly, an altered sensitivityof the nerves, which become more reactive, including the sequenceof sprouting and secondly, there may be onset of caries progression(Figure 5). Taken together, the bacteria may play a role in severedentin hypersensitivity, where only improved professional cleaningof the cervical area may lead to significant and permanent painrelief (48).
Iatrogenic development of hypersensitivity
During excavation the clinician may overextend the cavity preparationhereby exposing sound dentin (Figure 6), where the permeabilityof the dentinal tubules is higher than in subjacent carious dentin.This scenario may be accompanied with suboptimal cooling and dehydrationof the dentin. Consequently, the patient may experience severe dentinhypersensitivity following excavation and restoration.
The role of pulpal inflammation in dentin sensitivity
Pulpal A- and C-fibers can be sensitized by many external irritants, whichcan induce an inflammatory response in the pulp tissue. Sproutingof the nociceptive nerve terminals takes place in response to inflammationand may widen the receptive fields of the nerve fibers (43, 49),which may result in increased overlap of the receptive fields (=the area where a single neuron can be activated, when stimulated).Thus, stimulation of a small spot e.g. in dentin may result in activationof a much greater number of pulpal nociceptors and, consequently,increased sensitivity compared to a non-inflamed tooth (Figure 7).Moreover, inflammation and the consequent sprouting of the axonsmay result in more extensive innervation in pulp and pulp-dentinareas which are normally sparsely innervated in healthy teeth. Thismay be one mechanism playing a significant role in increased cervicalsensitivity (Figure 4). Also, fillings with open margins can inducepulpal inflammation, affecting the sensitivity of dentin in otherparts of the pulp. Open dentinal tubules next to such a fillingmay allow the diffusion and penetration of external irritants intothe pulp, resulting in inflammation, activation and also sproutingof the nerve endings in the pulp-dentin complex (Figure 8). In fact,it may well be that inflammation of some degree could in generalplay a role in dentin hypersensitivity.
In addition, dental pulp seems to contain a considerable number ofso called "silent" or "sleeping" nociceptors that cannot be activatedin healthy, but only in inflamed teeth (43). Electrophysiologicalexperiments indicate that approximately 40 % of the nociceptiveafferents can be activated in healthy teeth, whereas the proportionwill increase to 60 % when the pulp is inflamed. Considering thetotal number of the intradental afferents (approximately 1000) ineach tooth, such an increase in number of nociceptors is significantregarding the dental pain sensitivity.
Silent and "hot tooth«
It seems that the activation of pulpal nociceptors can vary toa great extent (5, 43, 50). In many cases acute pulpitis can beextremely painful. However, most often pulpal inflammation may proceedto total pulp necrosis with minor symptoms or with no symptoms at all(23, 50, 51) (Figure 3). This is puzzling considering the rich nociceptiveinnervation of the pulp. Such a variation in the symptoms can alsobe a serious diagnostic problem from the clinical point of view.A number of local mediators may be involved in the prevention ofthe nerve activation (43, 51). Those include e.g. local opioids,somatostatin, noradrenalin and nitric oxide (43, 52 - 54). These mediatorsare also important for regulation of the intensity of pulpal inflammation.The inhibition of nociceptor activity results in reduced releaseof the neuropeptides and other inflammatory mediators and also attenuationor even complete prevention of pain symptoms (43, 51). In additionto the local or peripheral sensitization and inhibition describedabove, mechanisms on brainstem level or higher in the central nervoussystem the complex nociceptive pathways may play an important roleto regulate the pain (central sensitization/inhibition), like inall pain development and modulation (55) .
Clinical cases of pulpal and dentinal pain andtheir treatment
Treatment of dentin hypersensitivity
With reference to classical literature, the clinical impressionand interpretation of dentin pain is something that will be triggeredand provoked by well-defined external stimuli. In the followingclinical scenarios, the accumulation of biofilm plays a huge rolein leading to pain.
The patient has not visited the dentist for years. The patientis completely unable to drink or have cold or hot fluids in theoral cavity due to pain. Clinically, the patient has a poor hygienestatus and a high number of defective restorations. Accumulationof biomasses is noted during the clinical examination. Not onlyare the restorations suboptimal, but also larger parts of the teethare broken down with exposed dentin. This has created an ecosystemwith biofilm formation on exposed dentin (Figure 9a, b). Followingseveral visits with only professional biofilm removal (Figure 9c),the patient arrives with a marked decrease in the pain level. Ofcourse, in the real life scenario the clinician would initiate bothhygiene procedures and restorations, but the present case reflectsthe important impact of biomasses on exposed dentin and dentin hypersensitivity.
If improved hygiene procedures has been introduced, but without painrelief the treatment plan should aim to reducing dentin permeability(Table 2). This can be achieved by either physically blocking thedentinal tubules or by depolarizing the nerves (56). A wide rangeof materials for desensitization have been sold but without universalsuccess. Dentin hypersensitivity can be very difficult to control,indicating that the materials either have no permanent effect and/orthat the inflammatory changes are so profound that a natural healingprocess is prevented. Several treatment modalities have shown anoccluding or desensitizing effect in animals, but it has been difficultto demonstrate in the clinic (56). A problem with materials thatare intended to block fluid flow in dentinal tubules, for exampleby precipitation of salt crystals, is that the precipitation maybe washed out, is dissolved in an acid medium or is worn away sothat the potential occluding effect is temporary.
There are many published studies on toothpastes with strontium saltsand potassium salts (57). Several of these report that these toothpasteshave some desensitizing effect, whereas others have not been ableto demonstrate an effect. The design of these studies have beenquestioned and the effect is uncertain (58). Before conducting acostly and invasive treatment, a practical test could be to evaluate whetherthe individual patient feels improvement in symptoms using thesetoothpastes. A paste consisting of arginine and calcium carbonate,claimed to close the dentinal tubuli, has been introduced as a gentletreatment of a sensitive area. So far, only preliminary resultsare available from the manufacturer (59, 60).
If the above methods are ineffective the next step would be to sealthe dentinal tubules with fluoride varnish, dentin primer and resinor with a resin restoration. In some cases it may end with endodontictreatment. As in other contexts, primary prevention is of coursethe optimal solution, by using a gentle brushing technique as wellas a low intake of soft drinks with low pH as opposed to the attemptto treat the established hypersensitive area/lesion.
Diagnosis and management of dentinal pain is often a challengeto the clinician. The dental pulp is exceptionally richly innervatedby nociceptive afferents, and pulpal and dentinal pain can causepatients considerable discomfort. Many factors are involved in thedevelopment and persistence of pain. Caries, iatrogenic damage, changesin dentin structure and permeability caused by erosion or toothwear, aggregation of biofilm on unprotected dentin; all can leadto activation of nociceptive nerves which initiates local inflammatorychanges in the pulp, and also triggers central changes in pain processing- both of which are complex and may be difficult to reverse.
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DDS, PhD, Professor in Oral Physiology, Departmentof Dentistry/Physiology, Institute of Medicine, University of EasternFinland, Finland
Associate professor, PhD, Dr.Odont. Department ofCariology and Endodontics, Faculty of Health and Medical Sciences,University of Copenhagen, Denmark
DDS, Dr. Odont. Senior Lecturer. Department of Endodonticsand Department of Orofacial Pain and Jaw Function, Faculty of Odontology,Malmö University, Malmö, Sweden
DDS, PhD, Professor. Department of Clinical Dentistry,Faculty of Medicine and Dentistry, University of Bergen, NORWAY
DDS, Dr. Odont. Associate Professor and Head, Section forEndodontics
Department of Clinical Dentistry, Faculty of Medicine and Dentistry.University of Bergen, Norway
Corresponding author: Matti Nähri, e-mail: firstname.lastname@example.org
This paper has been peer reviewed.
Närhi M, Bjørndal L, Pigg M, Fristad I, Haug SR. Acute dental painI: pulpal and dentinal pain. Nor Tannlegeforen Tid. 2016; 126: 10-8.
Pulpitis is a condition that causes painful inflammation of the pulp. It can occur in one or more teeth, and is caused by bacteria that invade the tooth's pulp, causing it to swell. There are two forms of pulpitis: reversible and irreversible.Which ganglion is associated with dental pain? ›
Trigeminal ganglion (TG) is known to be involved in pain caused by dental injury with most of its neuroinflammatory responses being similar to that observed in hyperalgesia or altered anesthesia in other inflamed tissues2.Is pulpal pain localized? ›
The myelinated axons have a fast conduction speed and low stimulation threshold, are superficial (located in the pulp and dentin junction), transmit pain directly to the thalamus, and generate a sharp and stabbing pain that is easily localized.What causes dentinal pain? ›
A toothache or tooth pain is caused when the nerve in the root of a tooth or surrounding a tooth is irritated. Dental (tooth) infection, decay, injury, or loss of a tooth are the most common causes of dental pain. Pain may also occur after an extraction (tooth is pulled out).What is symptoms of acute pulpitis? ›
Toothache and sensitivity are the main symptoms of pulpitis. The pain you feel usually varies depending on the stage of the inflammation. Symptoms of reversible pulpitis include: No pain when your dentist taps the tooth.Can antibiotics treat pulpitis? ›
Apart from removal of the tooth, the customary way of relieving the pain of irreversible pulpitis is by drilling into the tooth, removing the inflamed pulp (nerve) and cleaning the root canal. However, a significant number of dentists continue to prescribe antibiotics to stop the pain of irreversible pulpitis.What is the most common symptom of pulpal nerve damage? ›
- Tooth pain when biting down.
- Tooth pain while chewing.
- Sudden pain for no reason.
- Oversensitivity of the teeth with hot or cold drinks.
- Facial swelling.
Dental procedures: Multiple or unsuccessful dental procedures can make a tooth more susceptible to pulp necrosis. Trauma: An injury to your tooth can expose the pulp. It can also affect blood supply to the pulp, causing tissue death. Worn tooth enamel: This can be a result of aggressive brushing or grinding your teeth.What nerve is responsible for feeling a toothache? ›
Pain in the trigeminal system, including dental pain, is 'special'. Not only is the trigeminal nerve the largest sensory nerve in the body, represented by over 50% of the sensory cortex, but it is the only sensory nerve with an intracranial distal root ganglion: the trigeminal ganglion.What nerve causes dental pain? ›
As the pain caused by trigeminal neuralgia is often felt in the jaw, teeth or gums, many people with the condition visit a dentist before going to a GP.
By far the most common forms of oral pain are the acute form of pains that tend to last for short periods of time. These include toothache (dental pulpitis), gum pain (pericoronitis in 80% of the population), periapical periodontitis (owing to apical infection or postendodontic therapy of high occlusal contact).Can you feel pain in dentin? ›
Dentin hypersensitivity is characterized by brief sharp pain arising from exposed dentin in response to stimuli (typically thermal, evaporative, tactile, osmotic or chemical) that cannot be ascribed to any other form of dental defect or pathology.What are the three types of dentin? ›
- Primary dentine forms before tooth eruption.
- Secondary dentine forms after eruption, as the tooth develops with age. ...
- Reparative or tertiary dentine forms as a result of trauma to the odontoblasts; this can be thermal, chemical, bacterial or mechanical.
On average, a tooth nerve pain can last from as little as just a few days to as long as 4-6weeks or, in some instances, even longer. Considering the numbness ad sharp pain that may occur with a tooth nerve, you have to do what you can to get rid of the pain as soon as possible.How do you fix dentin pain? ›
In most cases, quick treatment options will solve the problem, including the use of desensitizing toothpaste, switching to a soft-bristled toothbrush, starting a daily fluoride rinse treatment, or minimizing teeth grinding with the help of a custom mouthguard.How can I relieve pulpitis pain? ›
Over-the-Counter Pain Relievers for Pulpitis
When taken in normal doses, NSAIDs (nonsteroidal anti-inflammatory drugs) like ibuprofen or non-opioid analgesics like acetaminophen can help manage the pain of pulpitis. Higher doses may be needed to reduce inflammation. These drugs are a good option for most people.
The most common first-line treatment for reducing pain is over-the-counter potassium nitrate dentifrice, which aims to desensitize the teeth by reducing nerve excitability.What antibiotics treat pulpitis? ›
Antibiotics are not recommended in the treatment of irreversible pulpitis! There is insufficient scientific research to ascertain whether the use of antibiotics is helpful, studies show that antibiotics do not have any significant effect of reducing the pain from a toothache.How do you test for pulpitis? ›
Cold spray applied to a Q-tip and then held on a tooth for 5-10 seconds. Assuming pain is produced by this cold stimulation, if the pain lingers for more than 10 seconds after the Q-tip is removed this is considered evidence of irreversible pulpitis.How do dentists treat pulpitis? ›
Treatment involves removing decay, restoring the damaged tooth, and sometimes doing root canal therapy or extracting the tooth. Reversible: Pulpitis begins as limited inflammation, and the tooth can be saved by a simple filling.
Amoxicillin is usually the first choice for tooth infection treatment. If your tooth infection is more serious, your dentist may prescribe a combination of amoxicillin and another drug called Clavulanate. This combination is stronger and more effective against tooth infections.Is pulpitis life threatening? ›
Is Pulpitis Dangerous? Pulpitis can be dangerous if left untreated. This is because it can quickly spread infection to other parts of the body, leading to other medical complications.How do I know if my tooth pulp is infected? ›
- Severe, constant, throbbing toothache that can spread to your jawbone, neck or ear.
- Pain or discomfort with hot and cold temperatures.
- Pain or discomfort with the pressure of chewing or biting.
- Swelling in your face, cheek or neck that may lead to difficulty breathing or swallowing.
Determining the risk of nerve damage with proper imaging is critical. A panorex and CBCT scan is done to determine the level of risk during an extraction. If a tooth is considered high risk then a coronectomy is indicated. A coronectomy is the removal of the entire crown of the third molar, leaving the roots in place.How do I know if my dentist caused nerve damage? ›
- Numbness or lack of feeling in the gums, cheeks, jaw, face, or tongue.
- A tingling or pulling sensation in these areas.
- Pain or burning.
- A loss of the ability to taste.
- Difficulty eating due to one or more of the symptoms above.
- A dull ache near the gum line.
- Discomfort when eating.
- Pain following exposure to hot or cold temperatures.
- Acute pain targeting a single tooth.
- Pain that radiates throughout the mouth.
Both reversible and irreversible pulpitis cause pain in the gums, teeth, jaw and ear, though the pain caused by reversible pulpitis may be milder.Can damaged pulp heal? ›
The inflammation is usually reversible, but there are times when the inflammation isn't reversible, and the pulp can't heal itself. In either case, it's best to visit your dentist for treatment so they can help get you on the road to recovery.What could happen if dental pulp is infected? ›
It's essential to seek treatment as soon as possible at the first signs of pain, sensitivity, swelling or any type of inflammation. Bacteria from a tooth's infected pulp can spread to other areas, and untreated pulpitis can lead to other medical conditions like: Sinusitis. Meningitis.How can you tell the difference between trigeminal neuralgia and dental pain? ›
Pain or attacks of trigeminal neuralgia can be triggered by certain actions or movements. Dental Pain: It is a very monotonous pain. It is not like a sharp shooting pain (electric shock) of Trigeminal Neuralgia.
Trigeminal neuralgia symptoms may include one or more of these patterns: Episodes of severe, shooting or jabbing pain that may feel like an electric shock. Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth.Can a dentist diagnose trigeminal neuralgia? ›
Most people with symptoms of trigeminal neuralgia end up at the dentist's office or in the ER. But that might not get you the help you need in either place. Ask to see a neurologist, who can diagnose your condition and can attempt to treat it with medical therapy first.What are the 3 types of neuralgia? ›
- Postherpetic neuralgia. This type of neuralgia occurs as a complication of shingles and may be anywhere on the body. ...
- Trigeminal neuralgia. ...
- Glossopharyngeal neuralgia.
Constant pain in gums and teeth. Tenderness. Headaches.Can TMJ cause tooth pain? ›
TMJ is often caused by teeth grinding and can cause tooth pain. TMJ dysfunction can cause several uncomfortable symptoms, including headaches, earache, make your teeth hurt and neck and jaw pain. The issue can also cause pain in the teeth, often as a result of habitual grinding and clenching.What is the best dental pain reliever? ›
Over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil, Motrin IB, and generic) and naproxen (Aleve and generic), work particularly well against dental pain because they block the enzyme that causes your gums to become red and swollen, says Paul A.Why is tooth pain worse at night? ›
When you lie down to sleep, more blood is able to rush to your brain. More blood circulation means experiencing more tooth pain than if you were standing. This is because the increased blood flow exerts pressure on the painful tooth.How is dental pain measured? ›
- Visual Analogue Scales (VAS)
- Heft-Parker visual analog scale (HPS)
- Verbal rating scale (VRS)
- Numerical rating Scale (NRS)
- Faces Pain Scale (FPS)
- Wong-Baker Faces Pain Rating Scale (WBS)
- Full Cup Test (FCT)
Three major mechanisms of dentinal sensitivity have been proposed in the literature: Direct innervation theory. Odontoblast receptor. Fluid movement/hydrodynamic theory.Can dentin get infected? ›
Dentine becomes infected as a result of caries lesion formation on root surfaces and when lesions progress following cavitation of enamel lesions. However, this infection is unimportant because the driving force for lesion formation and progression is the overlying biofilm.
Dentin contains microscopic tubes. When enamel begins to wear down or gums recede, the dentin becomes exposed. Tooth sensitivity is caused by the stimulation of cells within these tubes, causing a sharp pain when the area is exposed to hot or cold temperatures from food or beverages, or even the from the air.What are the 2 types of pulp stones? ›
True stones are made up of dentine and lined by odontoblasts, whereas false pulp stones are formed from degenerating cells of the pulp that are mineralized. A third type, “diffuse” or “amorphous” pulp stones, is more irregular in shape . Based on the location, they can be embedded, adherent, and free .What is the difference between dentine and dentin? ›
dentin, also spelled dentine, in anatomy, the yellowish tissue that makes up the bulk of all teeth. It is harder than bone but softer than enamel and consists mainly of apatite crystals of calcium and phosphate.What is the scientific name of dentin? ›
Dentin (/ˈdɛntɪn/) (American English) or dentine (/ˈdɛnˌtiːn/ or /ˌdɛnˈtiːn/) (British English) (Latin: substantia eburnea) is a calcified tissue of the body and, along with enamel, cementum, and pulp, is one of the four major components of teeth.Can pulpitis be seen on xray? ›
A dentist can diagnose pulpitis from a person's symptoms, an examination of the teeth, and possibly X-rays.Is pulpitis worse at night? ›
If your tooth pain is severe and gets much worse at night then there is a chance you are suffering from pulpitis. Pulpitis occurs when tooth decay and infection spreads past the outer layers of the tooth, infecting the pulp – which consists of nerves and blood vessels.How should I sleep with severe toothache? ›
Sleep with your head elevated – Prop up a few pillows to prevent your blood flow from rushing to your head, making your tooth pain worse. Use a cold compress – A cold compress (or towel-wrapped ice pack) can reduce inflammation and numb the area.What does pulpal mean? ›
pulp·al ˈpəl-pəl. : of or relating to pulp especially of a tooth.How do you get rid of pulp pain? ›
Over-the-Counter Pain Relievers for Pulpitis
When taken in normal doses, NSAIDs (nonsteroidal anti-inflammatory drugs) like ibuprofen or non-opioid analgesics like acetaminophen can help manage the pain of pulpitis. Higher doses may be needed to reduce inflammation. These drugs are a good option for most people.
It usually is reversible and it goes away on it's own. However, if pulpitis pain is severe and doesn't go away you should consult a doctor.
The most common symptoms of damaged pulp include pain in your tooth, and swelling and a sensation of heat in your gums. Your dentist will examine the painful tooth and take X-rays to confirm the diagnosis.Do antibiotics help pulpitis? ›
Apart from removal of the tooth, the customary way of relieving the pain of irreversible pulpitis is by drilling into the tooth, removing the inflamed pulp (nerve) and cleaning the root canal. However, a significant number of dentists continue to prescribe antibiotics to stop the pain of irreversible pulpitis.What is dental pulp treatment? ›
Pulp treatment is like a root canal, but is typically performed on primary teeth. Root canal procedures are used to treat permanent teeth with nerve and pulp problems. There are two main types of pulp therapy procedures: pulpotomy and pulpectomy.What is the best painkiller for tooth pain? ›
“Anti-inflammatory drugs such as ibuprofen, Advil, Motrin or naproxen work well with dental pain because they reduce inflammation,” says Huang. Recent data has shown the combination of Advil (ibuprofen) and Tylenol (acetaminophen) is as effective as prescription opioids for tooth pain.Can salt water make toothache worse? ›
Salt water rinses help decrease swelling, therefore offering pain relief. Aids in Gum Health and Soothes Bleeding Gums — If you have irritated or bleeding gums caused by toothaches, gingivitis, or canker sores, a salt water rinse can help manage the pain.What painkiller is good for toothache? ›
- take painkillers, like ibuprofen or paracetamol (children under 16 should not take aspirin) – a pharmacist can advise you.
- try rinsing your mouth with salt water (children should not try this)
Sleep with your head elevated – Prop up a few pillows to prevent your blood flow from rushing to your head, making your tooth pain worse. Use a cold compress – A cold compress (or towel-wrapped ice pack) can reduce inflammation and numb the area.Is pulpitis always an infection? ›
Pulpitis occurs when a bacterial infection spreads to the pulp chamber of an infected tooth, causing tissue to become swollen, inflamed or irritated deep inside the affected tooth. Pain is caused because the infection puts pressure on the surrounding nerves, blood vessels and tissue inside the tooth.