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

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

Bjork defined posterior crossbite as a malocclusion where the buccal cusps of canine, premolar and molar of upper teeth occlude lingually to the buccal cusps of canine, premolar and molar of lower teeth. Posterior crossbite is often correlated to a narrow maxilla and upper dental arch. A posterior crossbite can be unilateral, bilateral, single-tooth or entire segment crossbite. Posterior crossbite has been reported to occur between 7–23% of the population. The most common type of posterior crossbite to occur is the unilateral crossbite which occurs in 80% to 97% of the posterior crossbite cases. Posterior crossbites also occur most commonly in primary and mixed dentition. This type of crossbite usually presents with a "functional shift of the mandible towards the side of the crossbite". Posterior crossbite can occur due to either skeletal, dental or functional abnormalities. One of the common reasons for development of posterior crossbite is the size difference between maxilla and mandible, where maxilla is smaller than mandible. Posterior crossbite can result due to

- Upper Airway Obstruction where people with "adenoid faces" who have trouble breathing through their nose. They have an open bite malocclusion and present with development of posterior crossbite.

- Prolong digit or suckling habits which can lead to constriction of maxilla posteriorly

- Prolong pacifier use (beyond age 4)

Patient with skeletal open bites that accompany dental open bites may have Adenoid faces or Long face syndrome. They are said to have what is known as "Hyperdivergent Growth Pattern" which includes characteristics such as:

- Increased Lower Anterior Facial Height

- Occlusal plane diverges after the 1st molar contact

- May accompany dental open bite

- Narrow nostrils with upturned nose

- Dolicofacial or Leptoprosopic face pattern

- Constricted maxillary arch

- Bilateral Posterior Crossbite

- High and narrow palatal vault

- Presence of crowding in teeth

- Mentalis muscle strain upon forcibly closing of lips

- Possible gummy smile with increased interlabial gap

Cephalometric analysis features of skeletal open bite may include:

- Increased Frankfurt-Mandibular Plane angle

- Steep Occlusal Plane Angle

- Increased SN-MP Angle

- Short Mandibular ramus

- Increased mandibular body length

- Downward and backward position of mandible

- Increased gonial angle

- Proclined upper incisors, retroclined or upright lower incisors

- Posterior part of maxilla is tipped downwards

- Posterior facial height equals 1/2 of anterior facial height

- Increased hard tissue Lower Anterior Facial Height

- Increased total anterior facial height

- Short mandibular ramus

Viken Sassouni developed Sassouni analysis which indicates that patient's with long face syndrome have 4 of their bony planes (mandibular plane, occlusal plane, palatal plane, SN plane) steep to each other.

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.

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.

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).

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.

As a result of the changes to the developing embryo, the symptoms are very pronounced features, especially in the face. Low-set ears are a typical characteristic, as in all of the disorders which are called branchial arch syndromes. The reason for this abnormality is that ears on a foetus are much lower than those on an adult. During normal development, the ears "travel" upward on the head; however, in Crouzon patients, this pattern of development is disrupted. Ear canal malformations are extremely common, generally resulting in some hearing loss. In particularly severe cases, Ménière's disease may occur.

The most notable characteristic of Crouzon syndrome is craniosynostosis, as described above; however it usually presents as brachycephaly resulting in the appearance of a short and broad head. Exophthalmos (bulging eyes due to shallow eye sockets after early fusion of surrounding bones), hypertelorism (greater than normal distance between the eyes), and psittichorhina (beak-like nose) are also symptoms. Additionally, external strabismus is a common occurrence, which can be thought of as opposite from the eye position found in Down syndrome. Lastly, hypoplastic maxilla (insufficient growth of the midface) results in relative mandibular prognathism (chin appears to protrude despite normal growth of mandible) and gives the effect of the patient having a concave face. Crouzon syndrome is also associated with patent ductus arteriosus (PDA) and aortic coarctation.

For reasons that are not entirely clear, most Crouzon patients also have noticeably shorter humerus and femur bones relative to the rest of their bodies than members of the general population. A small percentage of Crouzon patients also have what is called "Type II" Crouzon syndrome, distinguished by partial syndactyly.

Crouzon syndrome is an autosomal dominant genetic disorder known as a branchial arch syndrome. Specifically, this syndrome affects the first branchial (or pharyngeal) arch, which is the precursor of the maxilla and mandible. Since the branchial arches are important developmental features in a growing embryo, disturbances in their development create lasting and widespread effects.

This syndrome is named after Octave Crouzon, a French physician who first described this disorder. He noted the affected patients were a mother and her daughter, implying a genetic basis. First called "craniofacial dysostosis", the disorder was characterized by a number of clinical features. This syndrome is caused by a mutation in the fibroblast growth factor receptor II, located on chromosome 10.

Breaking down the name, "craniofacial" refers to the skull and face, and "dysostosis" refers to malformation of bone.

Now known as Crouzon syndrome, the characteristics can be described by the rudimentary meanings of its former name. What occurs is that an infant's skull and facial bones, while in development, fuse early or are unable to expand. Thus, normal bone growth cannot occur. Fusion of different sutures leads to different patterns of growth of the skull.

Examples include: trigonocephaly (fusion of the metopic suture), brachycephaly (fusion of the coronal suture), dolichocephaly (fusion of the sagittal suture), plagiocephaly (unilateral premature closure of lambdoid and coronal sutures), oxycephaly (fusion of coronal and lambdoidal sutures), Kleeblattschaedel (premature closure of all sutures).

Hearing and vision disorders occur in more than half of people with Down syndrome.

Vision problems occur in 38 to 80%. Between 20 and 50% have strabismus, in which the two eyes do not move together. Cataracts (cloudiness of the lens of the eye) occur in 15%, and may be present at birth. Keratoconus (a thin, cone-shaped cornea) and glaucoma (increased eye pressure) are also more common, as are refractive errors requiring glasses or contacts. Brushfield spots (small white or grayish/brown spots on the outer part of the iris) are present in 38 to 85% of individuals.

Hearing problems are found in 50–90% of children with Down syndrome. This is often the result of otitis media with effusion which occurs in 50–70% and chronic ear infections which occur in 40 to 60%. Ear infections often begin in the first year of life and are partly due to poor eustachian tube function. Excessive ear wax can also cause hearing loss due to obstruction of the outer ear canal. Even a mild degree of hearing loss can have negative consequences for speech, language understanding, and academics. Additionally, it is important to rule out hearing loss as a factor in social and cognitive deterioration. Age-related hearing loss of the sensorineural type occurs at a much earlier age and affects 10–70% of people with Down syndrome.

The rate of congenital heart disease in newborns with Down syndrome is around 40%. Of those with heart disease, about 80% have an atrioventricular septal defect or ventricular septal defect with the former being more common. Mitral valve problems become common as people age, even in those without heart problems at birth. Other problems that may occur include tetralogy of Fallot and patent ductus arteriosus. People with Down syndrome have a lower risk of hardening of the arteries.