Dental open bite occurs in patients where the anterior teeth fail to touch. However, this is not accompanied by the skeletal tendency of having an open bite. Thus this type of open bite may happen in patients who have horizontal or hypodivergent growth pattern. These patients have normal jaw growth and do not have the long face syndrome. The anterior open bite in these patients may be caused by Macroglossia, Tongue thrusting habit or digit sucking habits. Some of the characteristics of a dental open bite include:

- Normal lower anterior facial height

- Horizontal/Hypodivergent growth pattern

- Occlusal plane diverges after the premolar contact

- Under-eruption of the anterior incisors

- Over-eruption of the posterior incisors

- Proclined upper and lower incisors

- No vertical maxillary excess or gummy smile

- Presence of habits such as thumb sucking, tongue thrusting

- Spacing between anterior incisors due to their proclination

Posterior open bite is caused when posterior teeth such as molars or premolars fail to touch their counterpart tooth. This is more likely to occur in segments where there may be unilateral open bite or open bite related to one or more teeth. Failure of eruption of teeth either due to primary failure or mechanical obstruction during eruption phase can cause the open bite. Sometimes lateral tongue thrust may also prevent the eruption of the posterior teeth, thus eliminating this habit maybe key to eruption in those instances.

Unilateral crossbite involves one side of the arch. The most common cause of unilateral crossbite is a narrow maxillary dental arch. This can happen due to habits such as digit sucking, prolonged use of pacifier or upper airway obstruction. Due to the discrepancy between the maxillary and mandibular arch, neuromuscular guidance of the mandible causes mandible to shift towards the side of the crossbite. This is also known as Functional mandibular shift. This shift can become structural if left untreated for a long time during growth, leading to skeletal asymmetries. Unilateral crossbites can present with following features in a child

- Lower midline deviation to the crossbite side

- Class 2 Subdivision relationships

- Temporomandibular disorders

Other kinds of malocclusions can be due to tooth size or horizontal, vertical, or transverse skeletal discrepancies, including skeletal asymmetries. Long faces may lead to "open bite malocclusion", while short faces can be coupled to a "Deep bite malocclusion". However, there are many other more common causes for open bites (such as tongue thrusting and thumb sucking), and likewise for deep bites. Upper or lower jaw can be overgrown or undergrown, leading to Class II or Class III malocclusions that may need corrective jaw surgery or orthognathic surgery as a part of overall treatment, which can be seen in about 5% of the general population.

An anterior crossbite in a child with baby teeth or mixed dentition may happen due to either dental misalignment or skeletal misalignment. Dental causes may be due to displacement of one or two teeth, where skeletal causes involve either mandibular hyperplasia, maxillary hypoplasia or combination of both.

Malocclusion is a common finding, although it is not usually serious enough to require treatment. Those who have more severe malocclusions, which present as a part of Craniofacial Anomalies, may require orthodontic and sometimes surgical treatment (orthognathic surgery) to correct the problem. Correction of malocclusion may reduce risk of tooth decay and help relieve excessive pressure on the temporomandibular joint. Orthodontic treatment is also used to align for aesthetic reasons.

Malocclusions may be coupled with skeletal disharmony of the face, where the relations between the upper and lower jaws are not appropriate. Such skeletal disharmonies often distort sufferer's face shape, severely affect aesthetics of the face, and may be coupled with mastication or speech problems. Most skeletal malocclusions can only be treated by orthognathic surgery.

Overbite medically refers to the extent of vertical (superior-inferior) overlap of the maxillary central incisors over the mandibular central incisors, measured relative to the incisal ridges.

The term overbite does not refer to a specific condition, nor is it a form of malocclusion. Rather an absent or excess overbite would be a malocclusion. Normal overbite is not measured in exact terms, but as a proportion (approximately 30–50% of the height of the mandibular incisors) and is commonly expressed as a percentage.

Prognathism in humans can be due to normal variation among phenotypes. In human populations where prognathism is not the norm, it may be a malformation, the result of injury, a disease state or a hereditary condition. Prognathism is considered a disorder only if it affects mastication, speech or social function as a byproduct of severely affected aesthetics of the face.

Clinical determinants include soft tissue analysis where the clinician assesses nasolabial angle, the relationship of the soft tissue portion of the chin to the nose, and the relationship between the upper and lower lips; also used is dental arch relationship assessment such as Angle's classification.

Cephalometric analysis is the most accurate way of determining all types of prognathism, as it includes assessments of skeletal base, occlusal plane angulation, facial height, soft tissue assessment and anterior dental angulation. Various calculations and assessments of the information in a cephalometric radiograph allow the clinician to objectively determine dental and skeletal relationships and determine a treatment plan.

Prognathism is less prevalent in East Asians and Caucasians. It is not to be confused with micrognathism, although combinations of both may be found. It affects the middle third of the face, causing it to jut out, thereby increasing the facial area, similar in phenotype of archaic hominids and apes. Mandibular prognathism is a protrusion of the mandible, affecting the lower third of the face. Alveolar prognathism is a protrusion of that portion of the maxilla where the teeth are located, in the dental lining of the upper jaw. Prognathism can also be used to describe ways that the maxillary and mandibular dental arches relate to one another, including malocclusion (where the upper and lower teeth do not align). When there is maxillary and/or alveolar prognathism which causes an alignment of the maxillary incisors significantly anterior to the lower teeth, the condition is called an overjet. When the reverse is the case, and the lower jaw extends forward beyond the upper, the condition is referred to as retrognathia (reverse overjet).

Overbite is often confused with overjet, which is the distance between the maxillary anterior teeth and the mandibular anterior teeth in the anterior-posterior axis.

"Overbite" may also be used commonly to refer to Class II malocclusion or retrognathia, though this usage can be considered incorrect. This is where the mesiobuccal cusp of the maxillary first molar is situated anterior to the buccal groove of the mandibular first molar; in other words, the mandible (lower jaw) appears too far behind the maxilla. A person presenting with Class II malocclusion may exhibit excessive overbite as well, or may have the opposite problem, which is referred to as openbite (or apertognathia). In the case of apertognathia, the teeth do not overlap enough or at all. The upper teeth protrude past the lower teeth.

This type of failure of eruption takes place when the affected tooth is ankylosed to the bone around it. This is different than primary failure of eruption where the affected tooth/teeth were not ankylosed. In mechanical failure of eruption, affected tooth has partial or complete loss of PDL in a panoramic radiograph and teeth distal to affected tooth do not have this condition. On a percussion test, a tooth with mechanical failure of eruption will have a dull metallic sound.

Not all alveolar prognathism is anomalous, and significant differences can be observed among different ethnic groups.

Harmful habits such as thumb sucking or tongue thrusting can result in or exaggerate an alveolar prognathism, causing teeth to misalign. Functional appliances can be used in growing children to help modify bad habits and neuro-muscular function, with the aim of correcting this condition.

Alveolar prognathism can also easily be corrected with fixed orthodontic therapy. However, relapse is quite common, unless the cause is removed or a long-term retention is used.

The term primary failure of eruption was named by Dr. William Proffit and Dr. Katherine Vig in 1981. This type of failure of eruption has a genetic or familial background precursor as a cause. The prevalence is of PFE is about 0.06% in population. In this type of failure, teeth that are non-ankylosed fail to erupt in the mouth. These teeth do not have a precursor tooth that is blocking their path. These teeth tend to erupt partially but then fail to erupt as the time goes on. Profitt stated that only the posterior teeth are the ones to be affected and all the teeth which are distal to the affected tooth are also affected. Both permanent and primary teeth may equally be affected. This often results in posterior open bite in patients mouth who have primary failure of eruption. This phenomenon can occur in any quadrant of the mouth.

There are two types of primary failure of eruption. Type I involves failure of eruption of teeth distal to the most mesial affected tooth to be all same. Type II involves a greater eruption pattern, not complete, among the teeth distal to the most mesial affected tooth. It is difficult to diagnose between these two types of failure of eruption because 2nd molar does not erupt until a patient is 15 years of age. Plenty of times, patient's receive orthodontic care much before they turn 15 years old. Therefore, to properly diagnose between two types, a patient needs to be over 15 and a definitive proof of uneruption of 2nd molar is required.

Hair abnormalities are very prominent in majority of the cases of TDO. Kinky/curly hair that is unusually dry and easily sheds is present at birth. In 80% of cases, the hair has a more relaxed appearance by adolescence. The presence of this hair texture type is a defining characteristic between a diagnosis of TDO verses amelogenesis imperfecta with hypomaturation. Additionally, in TDO the nails are usually abnormally thin, brittle, and split frequently. Cranial deficiencies are marked by the presence of having a long skull relative to its width, or protrusive foreheads due to increased thickness of the cranial bones and premature closing of the associated sutures in the skull. The long bones in the body (arms, legs) are also abnormally long and tend to fracture very easily. Osteosclerosis, commonly seen in TDO cases is characterized by an increase in bone density, affecting the skull and the mastoid process located behind the jawbone on the skull, as well as a shortened ramus seen in people with TDO. There are no known pathological problems associated with hair and bone changes in people with this disease. Changes in the long bones tend to appear later in development, but changes in the teeth appear once the teeth being to form, called primary dentition. The hair and bone abnormalities are evaluated radiographically during initial diagnosis, and visually during the course of the disease. Radiographic exams may be repeated if there is suspect of fracture.

In the oral cavity 100% of people diagnosed with TDO have taurodontism which is characterized by vertically enlarged pulp chambers at the expense of the roots of the teeth; the floor of the pulp chamber and furcation is moved apically down. This is due to the failure of the Hertwig epithelial root sheath which maps the shape of the forming tooth roots during active differentiation. Amelogenesis imperfecta, an abnormal formation of the enamel or external layer of the crown of the tooth, may also be present where the tooth enamel may be thin or absent. There are several clinical subsets of amelogenesis imperfecta, but common to TDO is the hypoplastic-hypomaturation subtype; the hypomaturation-hypoplastic is less common in individuals with TDO. The difference between the 2 dominant subtypes is the changes seen in the enamel matrix, and the phenotypic type that predominates. The hypoplastic-hypomaturation type of amelogenesis imperfecta with TDO occurs where the tooth enamel depicts a generalized pitted pattern, with open contacts between the teeth as well as an open bite. A smaller amount of cases are of the hypomaturation-hypoplastic case type, in which the enamel structure is softer due to the under maturation of ameloblasts during development. Mandibular prognathism also called a severe underbite, is also a prominent feature in TDO. Prognathism defects are diagnosed based the level of severity that this condition interferes with being able to chew or speak properly.

Due to improper tooth development, TDO patients suffer from high rates of dental caries causing dental abscess. The under maturation of the enamel causes the tooth structure to be softer, and more susceptible to the effects of bruxism due to abnormalities in skeletal development. The oral abnormalities are evaluated by radiographs and visual examination. Oral radiographs are frequently repeated due to the high incidence of infection due to abnormal biting patterns seen in TDO cases.

Repair with cementum or dentin occurs after partial root resorption, fusing the tooth with the bone. It may occur following dental trauma, especially occlusal trauma, or after periapical periodontitis caused by pulp necrosis. Ankylosis itself is not a reason to remove a permanent tooth, however teeth which must be removed for other reasons are made significantly more difficult to remove if they are ankylosed.

While identifying the causes of tongue thrust, it is important to remember that the resting posture of the tongue, jaw, and lips are crucial to normal development of mouth and its structures. If tongue rests against the upper front teeth, the teeth may protrude forward, and adverse tongue pressure can restrict the development of the oral cavity. The tongue lies low in the mouth or oral cavity and is typically forwarded between upper and lower teeth. If tongue thrust behavior is not corrected, it may affect the normal dental development. The teeth may be pushed around in different directions during the growth of permanent teeth.

Ankylosis of deciduous teeth ("submerged teeth") may rarely occur. The most commonly affected tooth is the mandibular (lower) second deciduous molar. Partial root resorption first occurs and then the tooth fuses to the bone. This prevents normal exfoliation of the deciduous tooth and typically causes impaction of the permanent successor tooth. As growth of the alveolar bone continues and the adjacent permanent teeth erupt, the ankylosed deciduous tooth appears to submerge into the bone, although in reality it has not changed position. Treatment is by extraction of the involved tooth, to prevent malocclusion, periodontal disturbance or dental caries.

OMD refers to abnormal resting posture of the orofacial musculature, atypical chewing, and swallowing patterns, dental malocclusions, blocked nasal airways, and speech problems. OMD are patterns involving oral and/orofacial musculature that interferes with normal growth, development, or function of structures, or calls attention to itself. OMD are found in both children and adults. OMD that are commonly seen in children include tongue thrust that is also known as swallowing with an anterior tongue posture. OMD also refers to factors such as nonnutritive sucking behaviors, such as thumb sucking, clenching, bruxing, etc. that led to abnormal development of dentition and oral cavity. OMD in adult and geriatric population are due to various neurological impairments, oral hygiene, altered functioning of muscles due to aging, systemic diseases, etc.

Tongue thrusting is a type of orofacial myofunctional disorder, which is defined as habitual resting or thrusting the tongue forward and/or sideways against or between the teeth while swallowing, chewing, resting, or speaking. Abnormal swallowing patterns push the upper teeth forward and away from the upper alveolar processes and cause open bites. In children, tongue thrusting is common due to immature oral behavior, narrow dental arch, prolonged upper respiratory tract infections, spaces between the teeth (diastema), muscle weakness, malocclusion, abnormal sucking habits, and open mouth posture due to structural abnormalities of genetic origin. Large tonsils and adenoids also contribute to tongue thrust swallowing.

From the dental perspective, teeth move in relation to the balance of the soft tissue; the normal relationship of teeth lies in occlusion; and any deviation from the normal occlusion can lead to dental distress. Tongue posture plays an important role in swallowing and dentofacial growth. In case of tongue thrust swallowing, the tip of the tongue can come against or between the dentition; the midpoint may be collapsed or extended unilaterally or bilaterally; or the posterior part of the hard palate. In these conditions, there are chances of abnormal dentofacial growth and other concerns regarding development of the craniofacial complex.

There are pertinent symptomatic questions that can be considered for the diagnosis of tongue thrust swallow. Some of these questions are geared toward tongue protrusion and an opening of lips when the client is in repose; habitual mouth breathing; digit sucking; existence of high and narrow palatal arch; ankyloglossia (tongue-tie); malocclusions, (Class II, III); weak chewing muscles (masseter); weak lip muscles (orbicularis oris); overdeveloped chin muscles (mentalis); muscular imbalance; abnormal dentition.

Tongue thrusting and speech problems may co-occur. Due to unconventional postures of the tongue and other articulators, interdental and frontal lisping are very common. The alveolar sounds /s/ and /z/ are produced more anteriorly thus leading to interdental fricative like sounds, /th/.

Although it may be asymptomatic, symptoms usually are more likely to be present and more severe with larger tongue enlargements. Signs and symptoms include:

- Dyspnea - difficult, noisy breathing, obstructive sleep apnea or airway obstruction

- Dysphagia - difficulty swallowing and eating

- Dysphonia - disrupted speech, possibly manifest as lisping

- Sialorrhea - drooling

- Angular cheilitis - sores at the corners of the mouth

- Crenated tongue - indentations on the lateral borders of the tongue caused by pressure from teeth ("pie crust tongue")

- Open bite malocclusion - a type of malocclusion of the teeth

- Mandibular prognathism - enlarged mandible

- Mouth breathing

- Orthodontic abnormalities - including diastema and tooth spacing

A tongue that constantly protrudes from the mouth is vulnerable to drying out, ulceration, infection or even necrosis.

Lefort I - Slight swelling of the upper lip, ecchymosis is present in the buccal sulcus beneath each zygomatic arch, malocclusion, mobility of teeth. Impacted type of fractures may be almost immobile and it is only by grasping the maxillary teeth and applying a little firm pressure that a characteristic grate can be felt which is diagnostic of the fracture. Percussion of upper teeth results in cracked pot sound. Guérin's sign is present characterised by ecchymosis in the region of greater palatine vessels.

Lefort II and Lefort III (common) - Gross edema of soft tissue over the middle third of the face, bilateral circumorbital ecchymosis, bilateral subconjunctival hemorrhage, epistaxis, CSF rhinorrhoea, dish face deformity, diplopia, enophthalmos, cracked pot sound.

Lefort II - Step deformity at infraorbital margin, mobile mid face, anesthesia or paresthesia of cheek.

Lefort III - Tenderness and separation at frontozygomatic suture, lengthening of face, depression of ocular levels (enophthalmos), hooding of eyes, and tilting of occlusal plane, an imaginary curved plane between the edges of the incisors and the tips of the posterior teeth. As a result, there is gagging on the side of injury.

Overjet is the extent of horizontal (anterior-posterior) overlap of the maxillary central incisors over the mandibular central incisors. In class II (division I) malocclusion the overjet is increased as the maxillary central incisors are protruded.

Diagnosis is suspected by physical exam and history, in which, classically, the hard and soft palate of the midface are mobile with respect to the remainder of facial structures. This finding can be inconsistent due to the midfacial bleeding and swelling that typically accompany such injuries, and so confirmation is usually needed by radiograph or CT.

Amelogenesis imperfecta (AI) is a congenital disorder that presents with a rare abnormal formation of the enamel or external layer of the crown of teeth, unrelated to any systemic or generalized conditions. Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it. Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel (ameloblastin, enamelin, tuftelin and amelogenin) as a result of abnormal enamel formation via amelogenesis.

People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey; this disorder can afflict any number of teeth of both dentitions. The teeth have a lower risk for dental cavities and are hypersensitive to temperature changes as well as rapid attrition, excessive calculus deposition, and gingival hyperplasia.

Most people who brux are unaware of the problem, either because there are no symptoms, or because the symptoms are not understood to be associated with a clenching and grinding problem. The symptoms of sleep bruxism are usually most intense immediately after waking, and then slowly abate, and the symptoms of a grinding habit which occurs mainly while awake tend to worsen through the day, and may not be present on waking. Bruxism may cause a variety of signs and symptoms, including:

- Excessive tooth wear, particularly attrition, which flattens the occlusal (biting) surface, but also possibly other types of tooth wear such as abfraction, where notches form around the neck of the teeth at the gumline.

- Tooth fractures, and repeated failure of dental restorations (fillings, crowns, etc.).

- Hypersensitive teeth, (e.g. dental pain when drinking a cold liquid) caused by wearing away of the thickness of insulating layers of dentin and enamel around the dental pulp.

- Inflammation of the periodontal ligament of teeth, which may make them sore to bite on, and possibly also a degree of loosening of the teeth.

- A grinding or tapping noise during sleep, sometimes detected by a partner or a parent. This noise can be surprisingly loud and unpleasant, and can wake a sleeping partner. Noises are rarely associated with awake bruxism.

- Other parafunctional activity which may occur together with bruxism: cheek biting (which may manifest as morsicatio buccarum and/or linea alba), and/or lip biting.

- A burning sensation on the tongue (see: glossodynia), possibly related to a coexistent "tongue thrusting" parafunctional activity.

- Indentations of the teeth in the tongue ("crenated tongue" or "scalloped tongue").

- Hypertrophy of the muscles of mastication (increase in the size of the muscles that move the jaw), particularly the masseter muscle.

- Tenderness, pain or fatigue of the muscles of mastication, which may get worse during chewing or other jaw movement.

- Trismus (restricted mouth opening).

- Pain or tenderness of the temporomandibular joints, which may manifest as preauricular pain (in front of the ear), or pain referred to the ear (otalgia).

- Clicking of the temporomandibular joints.

- Headaches, particularly pain in the temples, caused by muscle pain associated with the temporalis muscle.

Bruxism is usually detected because of the effects of the process (most commonly tooth wear and pain), rather than the process itself. The large forces that can be generated during bruxism can have detrimental effects on the components of masticatory system, namely the teeth, the periodontium and the articulation of the mandible with the skull (the temporomandibular joints). The muscles of mastication that act to move the jaw can also be affected since they are being utilized over and above of normal function.

AI can be classified according to their clinical appearances:

- Type 1 - Hypoplastic

Enamel of abnormal thickness due to malfunction in enamel matrix formation. Enamel is very thin but hard & translucent, and may have random pits & grooves. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel differs in appearance from dentine radiographically as normal functional enamel.

- Type 2 - Hypomaturation

Enamel has sound thickness, with a pitted appearance. It is less hard compared to normal enamel, and are prone to rapid wear, although not as intense as Type 3 AI. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel appears to be comparable to dentine in its radiodensity on radiograpshs.

- Type 3 - Hypocalcified

Enamel defect due to malfunction of enamel calcification, therefore enamel is of normal thickness but is extremely brittle, with an opaque/chalky presentation. Teeth are prone to staining and rapid wear, exposing dentine. Condition is of autosomal dominant and autosomal recessive pattern. Enamel appears less radioopaque compared to dentine on radiographs.

- Type 4: Hypomature hypoplastic enamel with taurodontism

Enamel has a variation in appearance, with mixed features from Type 1 and Type 2 AI. All Type 4 AI has taurodontism in common. Condition is of autosomal dominant pattern.

Other common features may include an anterior open bite, taurodontism, sensitivity of teeth.

Differential diagnosis would include dental fluorosis, molar-incisor hypomineralization, chronological disorders of tooth development.