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Pulp sensibility tests are routinely used in the diagnosis of dental disease. There are 2 general types:
- Thermal-- most commonly, ethyl chloride sprayed onto a small ball of cotton wool, which produces intense cold. Alternatively gutta percha can be heated to produce heat.
- Electrical pulp test-- electric pulp testing (EPT) has been available for over a century and used by dentists worldwide. It is used to determine the health of the pulp and pulp-related pain. It does not provide information on vascular supply to the pulp. EPT produces electrical stimuli that cause an ionic change across the neural membrane, inducing an action potential in myelinated nerves. The threshold of pain level will be determined by increasing the voltage. The requirements of an EPT are appropriate application method, careful interpretation of the results, and an appropriate stimulus. The tests must be done with tooth isolation and conduction media. EPT is not recommended for patients with orthodontic bands or crowned teeth. Key factors in testing are the enamel and dentine thickness and the number of nerve fibers underlying the pulp. Pulp nerve fibers respond to lower current intensities and a small number of pulpal afferents, creating neural responses when electrical stimulation is applied. EPTs may be unreliable and lead to false-positive and false-negative results. False-positive responses in teeth may be attributed to pulpal necrosis. Also, since pulpal and periodontal nerve thresholds may overlap, the periodontal nerves may give a false indication in tooth sensibility.
Possible explanations for false-positives include:
- Response caused by conduction of the current because of periodontal or gingival issues
- Breakdown products associated with pulp necrosis may be able to conduct electric current next to infected and hypersensitive pulp tissue
- Inflamed pulp tissue may still be present
- Metallic restorations or orthodontic gear are still present
Studies have indicated that there is little correlation between histopathological status of the pulp and clinical information. A negative EPT response showed localized necrosis in 25.7% of cases and 72% of cases. Thus, 97.7% of cases with a negative response to EPT indicated that a root canal treatment should be carried out.
Any tooth that is identified, in either the history of pain or base clinical exam, as a source for toothache may undergo further testing for vitality of the dental pulp, infection, fractures, or periodontitis. These tests may include:
- Pulp sensitivity tests, usually carried out with a cotton wool sprayed with ethyl chloride to serve as a cold stimulus, or with an electric pulp tester. The air spray from a three-in-one syringe may also be used to demonstrate areas of dentin hypersensitivity. Heat tests can also be applied with hot Gutta-percha. A healthy tooth will feel the cold but the pain will be mild and disappear once the stimulus is removed. The accuracy of these tests has been reported as 86% for cold testing, 81% for electric pulp testing, and 71% for heat testing. Because of the lack of test sensitivity, a second symptom should be present or a positive test before making a diagnosis.
- Radiographs utilized to find dental caries and bone loss laterally or at the apex.
- Assessment of biting on individual teeth (which sometimes helps to localize the problem) or the separate cusps (may help to detect cracked cusp syndrome).
Less commonly used tests might include trans-illumination (to detect congestion of the maxillary sinus or to highlight a crack in a tooth), dyes (to help visualize a crack), a test cavity, selective anaesthesia and laser doppler flowmetry.
The diagnosis of DH may be challenging. It is a diagnosis of exclusion, reached once all other possible explanations for the pain have been ruled out. A thorough patient history and clinical examination are required. The examination includes a pain provocation test by blasting air from a dental instrument onto the sensitive area, or gentle scratching with a dental probe. If a negative result for the pain provocation test occurs, no treatment for dentinal hypersensitivity is indicated and another diagnosis should be sought, such as other causes of orofacial pain.
Inflammation of the dental pulp, termed pulpitis, produces true hypersensitivity of the nerves in the dental pulp. Pulpitis is classified as "irreversible" when pulpal inflammation will irreversibly progress to pulpal necrosis due to compression of the venous microcirculation and tissue ischemia, and "reversible" when the pulp is still capable of returning to a healthy, non-inflamed state, although usually dental treatment is required for this. Irreversible pulpitis is readily distinguishable from DH. There is poorly localized, severe pain which is aggravated by thermal stimuli, and which continues after the stimulus is removed. There also is typically spontaneous pain without any stimulus. Reversible pulpitis may not be so readily distinguishable from DH, however usually there will be some obvious sign such as a carious cavity, crack, etc. which indicates pulpitis. In contrast to pulpitis, the pain of DH is short and sharp.
Once the pulp has become inflamed, the tooth can be diagnostically divided into two categories.
- Reversible pulpitis
- Irreversible pulpitis
Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin-pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e.g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms are likely to occur with or without any form of treatment, but they take time.
Since most toothache is the result of plaque-related diseases, such as tooth decay and periodontal disease, the majority of cases could be prevented by avoidance of a cariogenic diet and maintenance of good oral hygiene. That is, reduction in the number times that refined sugars are consumed per day and brushing the teeth twice a day with fluoride toothpaste and flossing. Regular visits to a dentist also increases the likelihood that problems are detected early and averted before toothache occurs. Dental trauma could also be significantly reduced by routine use of mouthguards in contact sports.
Prevention of pericoronitis can be achieved by removing impacted third molars before they erupt into the mouth, or through preemptive operculectomy. A treatment controversy exists about the necessity and timing of the removal of asymptomatic, disease-free impacted wisdom teeth which prevents pericoronitis. Proponents of early extraction cite the cumulative risk for extraction over time, the high probability that wisdom teeth will eventually decay or develop gum disease and costs of monitoring to retained wisdom teeth. Advocates for retaining wisdom teeth cite the risk and costs of unnecessary operations and the ability to monitor the disease through clinical exam and radiographs.
The diagnosis of cracked tooth syndrome is notoriously difficult even for experienced clinicians. The features are highly variable and may mimic sinusitis, temporomandibular disorders, headaches, ear pain, or atypical facial pain/atypical odontalgia (persistent idiopathic facial pain).
When diagnosing cracked tooth syndrome, a dentist takes many factors into consideration. A bite-test is commonly performed to confirm the diagnosis, in which the patient bites down on either a Q-tip, cotton roll, or an instrument called a Tooth Slooth.
Aetiology of CTS is multifactorial, the causative factors include:
- previous restorative procedures.
- occlusal factors
- developmental conditions/anatomical considerations.
- trauma
- others, e.g, aging dentition or presence of lingual tongue studs.
Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure.
The presence of dental plaque or infection beneath an inflamed operculum without other obvious causes of pain will often lead to a pericoronitis diagnosis; therefore, elimination of other pain and inflammation causes is essential. For pericoronal infection to occur, the affected tooth must be exposed to the oral cavity, which can be difficult to detect if the exposure is hidden beneath thick tissue or behind an adjacent tooth. Severe swelling and restricted mouth opening may limit examination of the area. Radiographs can be used to rule out other causes of pain and to properly assess the prognosis for further eruption of the affected tooth.
Sometimes a "migratory abscess" of the buccal sulcus occurs with pericoronal infection, where pus from the lower third molar region tracks forwards in the submucosal plane, between the body of the mandible and the attachment of the buccinator muscle to the mandible. In this scenario, pus may spontaneously discharge via an intra-oral sinus located over the mandibular second or first molar, or even the second premolar.
Similar causes of pain, some which can occur in conjunction with pericoronitis may include:
- Dental caries (tooth decay) of the wisdom tooth and of the distal surface of the second molar is common. Tooth decay may cause pulpitis (toothache) to occur in the same region, and this may cause pulp necrosis and the formation of a periapical abscess associated with either tooth.
- Food can also become stuck between the wisdom tooth and the tooth in front, termed food packing, and cause acute inflammation in a periodontal pocket when the bacteria become trapped. A periodontal abscess may even form by this mechanism.
- Pain associated with temporomandibular joint disorder and myofascial pain also often occurs in the same region as pericoronitis. They are easily missed diagnoses in the presence of mild and chronic pericoronitis, and the latter may not be contributing greatly to the individual's pain (see table).
It is rare for pericoronitis to occur in association with both lower third molars at the same time, despite the fact that many young people will have both lower wisdom teeth partially erupted. Therefore, bilateral pain from the lower third molar region is unlikely to be caused by pericoronitis and more likely to be muscular in origin.
Sometimes, pressure changes damage teeth (rather than just causing pain). When the external pressure rises or falls and the trapped air within the void cannot expand or contract to balance the external pressure, the pressure difference on the rigid structure of the tooth can occasionally induce stresses sufficient to fracture the tooth or dislodge a filling. Typically this is seen in underwater divers or aviators who experience pressure changes in the course of their activity. Identifying the pain during a pressure change is a diagnostic indicator for the clinician. Treatment involves removing the void space by carefully replacing the offending restoration, repeating the endodontic treatment or removing the tooth.
The Fédération dentaire internationale describes 4 classes of barodontalgia. The classes are based on signs and symptoms. They also provide specific and valuable recommendations for therapeutic intervention.
Treatment options include antibiotic therapy (not a permanent solution), endodontic (root canal) therapy, or extraction.
Periapical periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. Most epidemiologic data has been generated in European countries, especially Scandinavia. Millions of root canal treatments are carried out in the United States each year, although the total number of root canal treatments is an imperfect indicator of the prevalence of periapical periodontitis, since not always is it performed due to the presence of periapacial periodontitis, and not all cases of asymptomatic periodontitis will be treated in this manner, either due to lack of patient attendance or watchful waiting.
A periodontal abscess may be difficult to distinguish from a periapical abscess. Indeed, sometimes they can occur together. Since the management of a periodontal abscess is different from that of a periapical abscess, this differentiation is important to make.
- If the swelling is over the area of the root apex, it is more likely to be a periapical abscess; if it is closer to the gingival margin, it is more likely to be a periodontal abscess.
- Similarly, in a periodontal abscess pus most likely discharges via the periodontal pocket, whereas a periapical abscess generally drains via a parulis nearer to the apex of the involved tooth.
- If the tooth has pre-existing periodontal disease, with pockets and loss of alveolar bone height, it is more likely to be a periodontal abscess; whereas if the tooth has relatively healthy periodontal condition, it is more likely to be a periapical abscess.
- In periodontal abscesses, the swelling usually precedes the pain, and in periapical abscesses, the pain usually precedes the swelling.
- A history of toothache with sensitivity to hot and cold suggests previous pulpitis, and indicates that a periapical abscess is more likely.
- If the tooth which gives normal results on pulp sensibility testing, is free of dental caries and has no large restorations; it is more likely to be a periodontal abscess.
- A dental radiograph is of little help in the early stages of a dental abscess, but later usually the position of the abscess, and hence indication of endodontal/periodontal etiology can be determined. If there is a sinus, a gutta percha point is sometimes inserted before the x-ray in the hope that it will point to the origin of the infection.
- Generally, periodontal abscesses will be more tender to lateral percussion than to vertical, and periapical abscesses will be more tender to apical percussion.
Successful treatment of a dental abscess centers on the reduction and elimination of the offending organisms.
This can include treatment with antibiotics and drainage. If the tooth can be restored, root canal therapy can be performed. Non-restorable teeth must be extracted, followed by curettage of all apical soft tissue.
Unless they are symptomatic, teeth treated with root canal therapy should be evaluated at 1- and 2-year intervals after the root canal therapy to rule out possible lesional enlargement and to ensure appropriate healing.
Abscesses may fail to heal for several reasons:
- Cyst formation
- Inadequate root canal therapy
- Vertical root fractures
- Foreign material in the lesion
- Associated periodontal disease
- Penetration of the maxillary sinus
Following conventional, adequate root canal therapy, abscesses that do not heal or enlarge are often treated with surgery and filling the root tips; and will require a biopsy to evaluate the diagnosis.
The ICSD-R also described three different types of sleep bruxism according to the duration the condition is present, namely acute, which lasts for less than one week; subacute, which lasts for more than a week and less than one month; and chronic which lasts for over a month.
Research suggests that people with AFP are not helped greatly by health care professionals. One study reported that on average, individuals had consulted 7.5 different doctors. 91% had seen dentists, 80% physicians, 66% neurologists, 63% ear, nose and throat surgeons, 31% orthopedic and maxillofacial surgeons, 23% psychiatrists, 14% neurosurgeons and 6% ophalmologists and dermatologists. In this study, the individuals had been subjected to a wide variety of different treatments, from surgery, antidepressants, analgesics and physical therapies. None of the persons reported that surgery was beneficial, and in many cases the pain was worsened by surgery. The article sited as the source of this information was withdrawn from publication, saying the information was out of date and not meeting Cochrane methodological standards.
It has been suggested that the onset of chronic facial will likely be a life changing development for those affected.
The ICSD-R described three different severities of sleep bruxism, defining mild as occurring less than nightly, with no damage to teeth or psychosocial impairment; moderate as occurring nightly, with mild impairment of psychosocial functioning; and severe as occurring nightly, and with damage to the teeth, tempormandibular disorders and other physical injuries, and severe psychosocial impairment.
The ICHD-2 lists diagnostic criteria for "persistent idiopathic facial pain" (the term that replaces AFP in this classification):
There are presently no accepted medical tests which consistently discriminate between facial pain syndromes or differentiate Atypical Facial Pain from other syndromes. However, a normal Radiograph, CT, and MRI may help to exclude other pathology such as arterio-veinous malformation, tumor, temporomandibular joint disorder, or MS.
Diagnosis of mouth ulcers usually consists of a medical history followed by an oral examination as well as examination of any other involved area. The following details may be pertinent: The duration that the lesion has been present, the location, the number of ulcers, the size, the color and whether it is hard to touch, bleeds or has a rolled edge. As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon, or maxillofacial surgeon). If there have been previous ulcers which have healed, then this again makes cancer unlikely.
An ulcer that keeps forming on the same site and then healing may be caused by a nearby sharp surface, and ulcers that heal and then recur at different sites are likely to be RAS. Malignant ulcers are likely to be single in number, and conversely, multiple ulcers are very unlikely to be oral cancer. The size of the ulcers may be helpful in distinguishing the types of RAS, as can the location (minor RAS mainly occurs on non-keratinizing mucosa, major RAS occurs anywhere in the mouth or oropharynx). Induration, contact bleeding and rolled margins are features of a malignant ulcer. There may be nearby causative factor, e.g. a broken tooth with a sharp edge that is traumatizing the tissues. Otherwise, the person may be asked about problems elsewhere, e.g. ulceration of the genital mucous membranes, eye lesions or digestive problems, swollen glands in neck (lymphadenopathy) or a general unwell feeling.
The diagnosis comes mostly from the history and examination, but the following special investigations may be involved: blood tests (vitamin deficiency, anemia, leukemia, Epstein-Barr virus, HIV infection, diabetes) microbiological swabs (infection), or urinalysis (diabetes). A biopsy (minor procedure to cut out a small sample of the ulcer to look at under a microscope) with or without immunofluorescence may be required, to rule out cancer, but also if a systemic disease is suspected. Ulcers caused by local trauma are painful to touch and sore. They usually have an irregular border with erythematous margins and the base is yellow. As healing progresses, a keratotic (thickened, white mucosa) halo may occur.
Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.
It is normally possible to establish the cause of ear pain based on the history. It is important to exclude cancer where appropriate, particularly with unilateral otalgia in an adult who uses tobacco or alcohol.Often migraines are caused by middle ear infections which can easily be treated with antibiotics. Often using a hot washcloth can temporarily relieve ear pain.
For sinusitis lasting more than 12 weeks a CT scan is recommended. On a CT scan, acute sinus secretions have a radiodensity of 10 to 25 Hounsfield units (HU), but in a more chronic state they become thickened, with a radiodensity of 30 to 60 HU.
Nasal endoscopy and clinical symptoms are also used to make a positive diagnosis. A tissue sample for histology and cultures can also be collected and tested. Allergic fungal sinusitis (AFS) is often seen in people with asthma and nasal polyps. In rare cases, sinusoscopy may be made.
Nasal endoscopy involves inserting a flexible fiber-optic tube with a light and camera at its tip into the nose to examine the nasal passages and sinuses. This is generally a completely painless (although uncomfortable) procedure which takes between five and ten minutes to complete.
Health care providers distinguish bacterial and viral sinusitis by watchful waiting. If a person has had sinusitis for fewer than 10 days without the symptoms becoming worse, then the infection is presumed to be viral. When symptoms last more than 10 days or get worse in that time, then the infection is considered bacterial sinusitis. Imaging by either X-ray, CT or MRI is generally not recommended unless complications develop. Pain caused by sinusitis is sometimes confused for pain caused by pulpitis (toothache) of the maxillary teeth, and vice versa. Classically, the increased pain when tilting the head forwards separates sinusitis from pulpitis.