Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
By definition, BMS has no signs. Sometimes affected persons will attribute the symptoms to sores in the mouth, but these are in fact normal anatomic structures (e.g. lingual papillae, varices). Symptoms of BMS are variable, but the typical clinical picture is given below, considered according to the Socrates pain assessment method (see table). If clinical signs are visible, then another explanation for the burning sensation may be present. Erythema (redness) and edema (swelling) of papillae on the tip of the tongue may be a sign that the tongue is being habitually pressed against the teeth. The number and size of filiform papillae may be reduced. If the tongue is very red and smooth, then there is likely a local or systemic cause (e.g. eythematous candidiasis, anemia).
Several local and systemic factors can give a burning sensation in the mouth without any clinical signs, and therefore may be misdiagnosed as BMS. Some sources state that where there is an identifiable cause for a burning sensation, this can be termed "secondary BMS" to distinguish it from primary BMS. However, the accepted definitions of BMS hold that there are no identifiable causes for BMS, and where there are identifiable causes, the term BMS should not be used.
Some causes of a burning mouth sensation may be accompanied by clinical signs in the mouth or elsewhere on the body. For example, burning mouth pain may be a symptom of allergic contact stomatitis. This is a contact sensitivity (type IV hypersensitivity reaction) in the oral tissues to common substances such as sodium lauryl sulfate, cinnamaldehyde or dental materials. However, allergic contact stomatitis is accompanied by visible lesions and gives positive response with patch testing. Acute (short term) exposure to the allergen (the substance triggering the allergic response) causes non-specific inflammation and possibly mucosal ulceration. Chronic (long term) exposure to the allergen may appear as chronic inflammatory, lichenoid (lesions resembling oral lichen planus), or plasma cell gingivitis, which may be accompanied by glossitis and cheilitis. Apart from BMS itself, a full list of causes of an oral burning sensation is given below:
- Deficiency of iron, folic acid or various B vitamins (glossitis e.g. due to anemia), or zinc
- Neuropathy, e.g. following damage to the chorda tympani nerve.
- Hypothyroidism.
- Medications ("scalded mouth syndrome", unrelated to BMS) - protease inhibitors and angiotensin-converting-enzyme inhibitors (e.g. captopril).
- Type 2 diabetes
- True xerostomia, caused by hyposalivation e.g. Sjögren's syndrome
- Parafunctional activity, e.g. nocturnal bruxism or a tongue thrusting habit.
- Restriction of the tongue by poorly constructed dentures.
- Geographic tongue.
- Oral candidiasis.
- Herpetic infection (herpes simplex virus).
- Fissured tongue.
- Lichen planus.
- Allergies and contact sensitivities to foods, metals, and other substances (see table).
- Hiatal hernia.
- Human immunodeficiency virus.
- Multiple myeloma
The alterations in the sense of taste, usually a metallic taste, and sometimes smell are the only symptoms. The duration of the symptoms of dysgeusia depends on the cause. If the alteration in the sense of taste is due to gum disease, dental plaque, a temporary medication, or a short-term condition such as a cold, the dysgeusia should disappear once the cause is removed. In some cases, if lesions are present in the taste pathway and nerves have been damaged, the dysgeusia may be permanent.
Dysgeusia, also known as parageusia, is a distortion of the sense of taste. Dysgeusia is also often associated with ageusia, which is the complete lack of taste, and hypogeusia, which is a decrease in taste sensitivity. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary symptom. The distortion in the sense of taste is the only symptom, and diagnosis is usually complicated since the sense of taste is tied together with other sensory systems. Common causes of dysgeusia include chemotherapy, asthma treatment with albuterol, and zinc deficiency. Different drugs could also be responsible for altering taste and resulting in dysgeusia. Due to the variety of causes of dysgeusia, there are many possible treatments that are effective in alleviating or terminating the symptoms of dysgeusia. These include artificial saliva, pilocarpine, zinc supplementation, alterations in drug therapy, and alpha lipoic acid.
Dentin hypersensitivity (abbreviated to DH, or DHS, and also termed sensitive dentin, dentin sensitivity, cervical sensitivity, and cervical hypersensitivity) is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.
A degree of dentin sensitivity is normal, but pain is not usually experienced in everyday activities like drinking a cooled drink. Therefore, although the terms "dentin sensitivity" and "sensitive dentin" are used interchangeably to refer to dental hypersensitivity, the latter term is the most accurate.
The pain is sharp and sudden, in response to an external stimulus. The most common trigger is cold, with 75% of people with hypersensitivity reporting pain upon application of a cold stimulus. Other types of stimuli may also trigger pain in dentin hypersensitivity, including:
- Thermal – hot and cold drinks and foods, cold air, coolant water jet from a dental instrument.
- Electrical – electric pulp testers.
- Mechanical–tactile – dental probe during dental examination, periodontal scaling and root planing, toothbrushing.
- Osmotic – hypertonic solutions such as sugars.
- Evaporation – air blast from a dental instrument.
- Chemical – acids, e.g. dietary, gastric, acid etch during dental treatments.
The frequency and severity with which the pain occurs are variable.
Orofacial granulomatosis is enlargement of lips due to the formation of non-caseating granulomatous inflammation, which obstruct lymphatic drainage of the orofacial soft tissues, causing lymphedema. Essentially, granulomatous cheilitis refers to the lip swelling that accompanies this condition. "Median cheilitis" may be seen, which is fissuring in the midline of the lips due to the enlargement of the lips. Angular cheilitis may also be associated with orofacial granulomatosis.
A related condition is Melkersson–Rosenthal syndrome, a triad of facial palsy, chronic lip edema, and fissured tongue. "Miescher’s cheilitis", and "granulomatous macrocheilitis", are synonyms of granulomatous cheilitis.
Common causes of drug-related cheilitis include Etretinate, Indinavir, Protease inhibitors, Vitamin A and Isotretinoin (a retinoid drug). Uncommon causes include Atorvastatin, Busulphan, Clofazimine, Clomipramine, Cyancobalamin, Gold, Methyldopa, Psoralens, Streptomycin, Sulfasalazine and Tetracycline. A condition called "drug-induced ulcer of the lip" is described as being characterized by painful or tender, well-defined ulcerations of the lip without induration. It is the result of oral administration of drugs, and the condition resolves when the drugs are stopped.
Symptoms of otodental syndrome can and usually appear in early development and progress with age. Although the specific frequency of the symptoms is not known, the duration is recognized to be for life; assuming no treatment has been undergone. The symptoms are variable to each individual, can range greatly in severity and are dependent on gene expression.
More severe symptoms include:
- Globodontia – an abnormal condition that can occur in both primary and secondary tooth development, in which the molars and canines are greatly enlarged. It refers to the enlarged bulbous fused malformed posterior teeth with almost no discernible cusps or grooves. The molars are known to have a rounded globe-like shape. Can attribute to pain.
- Sensorineural hearing loss (SNHL) – also known as nerve related hearing loss, is a form of hearing loss associated with complications within the inner ear.
- Taurodontism – known as a condition in which the body of a tooth is enlarged at the expense of the roots. This results in an enlarged pulp chamber, lack of proper bonding at the cementoenamel junction, and can cause the pulpal floor to be displaced towards the root. Discomfort and pain are usually associated with these characteristics.
- Endodontic-Periodontic lesions – oral lesions that can potentially form into abscesses. May cause further soreness and pain.
Other possible, less severe, symptoms involve:
- Absent premolars – individuals suffering from otodental syndrome will typically lack the ability to develop premolars due to its genetic related affects.
- Ocular coloboma – an existent hole within the eye of the individual. The hole can be present in either the iris, choroid, optic disc, or retina and is acquired during early/prenatal development. Individuals with these symptoms may exhibit sensitivity to light, blurred vision, and/or blind spots; depending on the size of the missing tissue and its location in the eye.
Symptoms range in severity from mild to disabling.
Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.
A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic and/or anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth, dry eyes, and an overactive bladder.
Trismus is defined as difficulty in opening the mouth due to a muscle spasm resulting from a disturbance in the trigeminal nerve, however it can also refer to limited mouth opening of any cause. Another definition of trismus is simply a limitation of movement. Historically and commonly, the term "lock jaw" was sometimes used as a synonym for both trismus and tetanus.
Normal mouth-opening ranges from 35 to 45 mm. Males usually have slightly greater mouth opening than females. (40–60 mm, average of 35 mm). The Normal Lateral movement is 8-12mm, and normal protrusive movement is approximately 10mm. Some have distinguished mild trismus as 20–30 mm interincisal opening, moderate as 10–20 mm and severe as less than 10 mm.
Trismus is derived from the Irish word "trismos" meaning "a scream; a grinding, rasping or gnashing"
Otodental syndrome, also known as otodental dysplasia, is an exceptionally rare disease that is distinguished by a specific phenotype known as globodontia, that in rare cases can be associated with eye coloboma and high frequency hearing loss. Globodontia is an abnormal condition that can occur in both the primary and secondary dentition, except for the incisors which are normal in shape and size. This is demonstrated by significant enlargement of the canine and molar teeth. The premolars are either reduced in size or are absent. In some cases, the defects affecting the teeth, eye and ear can be either individual or combined. When these conditions are combined with eye coloboma, the condition is also known as oculo-otodental syndrome. The first known case of otodental syndrome was found in Hungary in a mother and her son by Denes and Csiba in 1969. Prevalence is less than 1 out of every 1 million individuals.
The cause of otodental syndrome is considered to be genetic. It is an autosomal dominant inheritance and is variable in its expressivity. Haploinsufficiency in the fibroblast growth factor 3 (FGF3) gene (11q13) has been reported in patients with otodental syndrome and is thought to cause the phenotype. Both males and females are equally affected. Individuals diagnosed with otodental syndrome can be of any age; age is not a relevant factor.
Currently there are no specific genetic treatments for otodental syndrome. Dental and orthodontic management are the recommended course of action.
Intermittent hair–follicle dystrophy is a disorder of the hair follicle leading to increased fragility of the shaft, with no identifiable biochemical disturbance, also with an unknown prevalence.
Trismus, also called lockjaw, is reduced opening of the jaws (limited jaw range of motion). It may be caused by spasm of the muscles of mastication or a variety of other causes. Temporary trismus occurs much more frequently than permanent trismus. It is known to interfere with eating, speaking, and maintaining proper oral hygiene. This interference, specifically with the patient's ability to swallow properly, results in an increased risk of aspiration. In some instances, trismus presents with altered facial appearance. The condition may be distressing and painful for the patient. Examination and treatments requiring access to the oral cavity can be limited, or in some cases impossible, due to the nature of the condition itself.
Multiple chemical sensitivity (MCS), also known as idiopathic environmental intolerances (IEI), is a disputed chronic condition characterized by symptoms that the affected person attributes to low-level exposures to commonly used chemicals. Symptoms are typically vague and non-specific. They may include fatigue, headaches, nausea, and dizziness.
Commonly attributed substances include scented products, pesticides, plastics, synthetic fabrics, smoke, petroleum products, and paint fumes.
Although the symptoms themselves are real, and can be disabling, MCS is not recognized as an organic, chemical-caused illness by the World Health Organization, American Medical Association, or any of several other professional medical organizations. Blinded clinical trials show that people with MCS react as often and as strongly to placebos as they do to chemical stimuli; the existence and severity of symptoms is related to perception that a chemical stimulus is present. Some attribute the symptoms to depression, somatoform disorders, or anxiety disorders.
Abrasion is a pathological, non-carious tooth loss that most commonly affects the premolars and canines. Abrasion frequently presents at the cemento-enamel junction and can be caused by many contributing factors, all with the ability to affect the tooth surface in varying degrees.
Sources of abrasion may arise from oral hygiene habits such as toothbrushes, toothpicks, floss, and dental appliance or may arise from other habits such as nail biting, chewing tobacco or another object. Abrasion can also occur from the type of dentifrice being utilized as some have more abrasive qualities such as whitening toothpastes.
The appearance may vary depending on the aetiology of abrasion, however most commonly presents in a V-shaped caused by excessive lateral pressure whilst tooth-brushing. The surface is shiny rather than carious, and sometimes the ridge is deep enough to see the pulp chamber within the tooth itself.
In order for successful treatment of abrasion to occur, the aetiology first needs to be identified and ceased, e.g. overzealous brushing. Once this has occurred subsequent treatment may involve the changes in oral hygiene or toothpaste, application of fluoride to reduce sensitivity or the placement of a restoration to aid in reducing the progression of further tooth loss.
There are no specific symptoms associated with claims of EHS and reported symptoms range widely between individuals. They include headache, fatigue, stress, sleep disturbances, skin prickling, burning sensations and rashes, pain and ache in muscles and many other health problems. In severe cases such symptoms can be a real and sometimes disabling problem for the affected person, causing psychological distress. There is no scientific basis to link such symptoms to electromagnetic field exposure.
The prevalence of some reported symptoms is geographically or culturally dependent and does not imply "a causal relationship between symptoms and attributed exposure". Many such reported symptoms overlap with other syndromes known as symptom-based conditions, functional somatic syndromes, and IEI (idiopathic environmental intolerance).
Those reporting electromagnetic hypersensitivity will usually describe different levels of susceptibility to electric fields, magnetic fields, and various frequencies of electromagnetic waves. Devices implicated include fluorescent and low-energy lights, mobile, cordless/portable phones, and WiFi. A 2001 survey found that people self-diagnosing as EHS related their symptoms most frequently to mobile phone base stations (74%), followed by mobile phones (36%), cordless phones (29%), and power lines (27%). Surveys of electromagnetic hypersensitivity sufferers have not been able to find any consistent pattern to these symptoms.
Opioid-induced hyperalgesia or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia is a phenomenon associated with the long-term use of opioids such as morphine, hydrocodone, oxycodone, and methadone. Over time, individuals taking opioids can develop an increasing sensitivity to noxious stimuli, even evolving a painful response to previously non-noxious stimuli (allodynia). Some studies on animals have also demonstrated this effect occurring after only a single high dose of opioids.
Tolerance, another condition that can arise from prolonged exposure to opioids, can often be mistaken for opioid-induced hyperalgesia and vice-versa, as the clinical presentation can appear similar. Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation to receive the same level of effect to treat pain, they are nevertheless caused by two distinct mechanisms. The similar net effect makes the two phenomena difficult to distinguish in a clinical setting. Under chronic opioid treatment, a particular individual's requirement for dose escalation may be due to tolerance, opioid-induced hyperalgesia, or a combination of both. In tolerance, there is a lower sensitivity to opioids, which occurs via two major theories: decreased receptor activation (desensitization of antinociceptive mechanisms), and opioid receptor down-regulation (internalization of membrane receptors). In opioid-induced hyperalgesia, sensitization of pronociceptive mechanisms occurs, resulting in a decrease in the pain threshold, or allodyna. Identifying the development of hyperalgesia is of great clinical importance since patients receiving opioids to relieve pain may paradoxically experience more pain as a result of treatment. Whereas increasing the dose of opioid can be an effective way to overcome tolerance, doing so to compensate for opioid-induced hyperalgesia may worsen the patient's condition by increasing sensitivity to pain while escalating physical dependence.
The phenomenon is common among palliative care patients following a too rapid escalation of opioid dosage.
Oromandibular Symptoms
- difficulty opening the mouth (trismus)
- clenching or grinding of the teeth (bruxism)
- spasms of jaw opening
- sideways deviation or protrusion of the jaw
- lip tightening and pursing
- drawing back (retraction) of the corners of the mouth
- deviation or protrusion of the tongue.
- jaw pain
- difficulties eating and drinking
- difficulties speaking (dysarthria)
Blepharospasm symptoms
- the first symptom to appear is an increased rate of blinking
- uncontrollable squinting/closing of eyes
- light sensitivity (photophobia)
- squinting/eyes closing during speech
- uncontrollable eyes closing shut (rare instances completely causing blindness)
In addition, in some patients, the dystonic spasms may sometimes be provoked by certain activities, such as talking, chewing, or biting. Particular activities or sensory tricks may sometimes temporarily alleviate OMD symptoms, including chewing gum, talking, placing a toothpick in the mouth, lightly touching the lips or chin, or applying pressure beneath the chin.
CGPD is characterized by the presence of small, raise, dome-shape papules primarily distributed around the mouth, eyes, and nose. Affected children may also have papules on the ears, eyelids, cheeks, forehead, and nose. CGPD skin lesions affecting areas of the skin other than the face are rare.
CGPD is known to be a temporary skin disease with a benign course. The skin papules typically resolve after a few months to a few years. After CGPD resolves, the skin may return to normal without scarring or may have small atrophic depressions with collagen loss, milia, or small pit-like scars.
The main symptom is pain, which often suddenly appears, is made worse by biting on the involved tooth, which may feel raised and prominent in the bite. The tooth may be mobile, and the lesion may contribute to destruction of the periodontal ligament and alveolar bone. The pain is deep and throbbing. The oral mucosa covering an early periodontal abscess appears erythematous (red), swollen and painful to touch. The surface may be shiny due to stretching of the mucosa over the abscess. Before pus has formed, the lesion will not be fluctuant, and there will be no purulent discharge. There may be regional lymphadenitis.
When pus forms, the pressure increases, with increasing pain, until it spontaneously drains relieving the pain. When pus drains into the mouth, a bad taste is perceived. Usually drainage occurs via the periodontal pocket, or else the infection may spread as a cellulitis or a purulent odontogenic infection. Local anatomic factors determine the direction of spread (see fascial spaces of the head and neck). There may be systemic upset, with malaise and pyrexia.
The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle. Some Meige's patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.
The condition tends to affect women more frequently than men.
Symptoms can range from mild to extreme—often described as extreme flu-like symptoms. Many symptoms may be associated with fungemia, including pain, acute confusion, chronic fatigue, and infections. Skin infections can include persistent or non-healing wounds and lesions, sweating, itching, and unusual discharge or drainage.
Electromagnetic hypersensitivity (EHS) is a claimed sensitivity to electromagnetic fields, to which negative symptoms are attributed. EHS has no scientific basis and is not a recognised medical diagnosis. Claims are characterized by a "variety of non-specific symptoms, which afflicted individuals attribute to exposure to electromagnetic fields".
Those who are self-described with EHS report adverse reactions to electromagnetic fields at intensities well below the maximum levels permitted by international radiation safety standards. The majority of provocation trials to date have found that such claimants are unable to distinguish between exposure and non-exposure to electromagnetic fields. A systematic review in 2005 showed no convincing scientific evidence for symptoms being caused by electromagnetic fields. Since then, several double-blind experiments have shown that people who report electromagnetic hypersensitivity are unable to detect the presence of electromagnetic fields and are as likely to report ill health following a sham exposure as they are following exposure to genuine electromagnetic fields, suggesting the cause in these cases to be the nocebo effect.
A 2005 review by the UK Health Protection Agency and a 2006 systematic review each evaluated the evidence for various medical, psychological, behavioral, and alternative treatments for EHS and each found that the evidence-base was limited and not generalizable, but that the best evidence favored cognitive behavioural therapy. As of 2005, WHO recommended that people presenting with claims of EHS be evaluated to determine if they have a medical condition that may be causing the symptoms the person is attributing to EHS, that they have a psychological evaluation, and that the person's environment be evaluated for issues like air or noise pollution that may be causing problems.
Some people who feel they are sensitive to electromagnetic fields may seek to reduce their exposure or use alternative medicine. Government agencies have enforced false advertising claims against companies selling devices to shield against EM radiation.