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The median alveolar cyst is a rare cyst, occurring in the bony alveolus between the maxillary central incisors. It is distinguished from a periapical cyst by the fact that adjacent teeth are vital.
Clinical examination and x rays can help diagnose the condition. For examples :
- Valsalva test (nose blowing test): Ask the patient to pinch the nostrils together and open the mouth, then blow gently through the nose. Observe if there is passage of air or bubbling of blood in the post extraction alveolus as the trapped air from closed nostrils is forced into the mouth through any oroantral communication. Gentle suction applied to the socket often produces a characteristic hollow sound.
- Perform a complete extra- and intra-oral examination using a dental mirror under good lighting, look for granulation tissue in the socket and openings into the antrum.
- Panoramic radiograph or paranasal computed tomography can help to locate the fistula, the size of it and to determine the presence of sinusitis and other foreign bodies. Other methods like radiographs (occipitomental, OPG and periapical views) can also be used to confirm the presence of any oroantral fistulas.
- To test the patency of communication the patient is asked to rinse the mouth or water is flushed in the tooth socket.
- Unilateral epistaxis is seen in case of collection of blood in the sinus cavity.
- Do not probe or irrigate the site, because it may lead to sinusitis or push foreign bodies, such as contaminated fragments, or oral flora further into the antrum. Hence, leading to the formation of a new fistula or widen an existing one.
The maxillary sinus is known for its thin floor walls and close proximity to the posterior maxillary teeth. Dental procedures such as extraction of these teeth sometimes cause OAC. The posterior maxillary molars and maxillary sinus are innervated by the same branch of nerves which is the maxillary division of trigeminal nerve. This innervation complicates the situation as the pain from maxillary sinus might be indistinguishable from a posterior maxillary toothache. Other known causes of OAC are fracture across the antral floor typically Le Fort I, displacement of posterior maxillary molar roots into antrum, and direct trauma. Extraction of primary teeth are not considered a risk of OAC due to the presence of developing permanent teeth and the small size of a developing maxillary sinus. OAC can happen for many other reasons, such as acute or chronic inflammatory lesions around the apex of tooth root present in close proximity with the maxillary antrum, necrotic lesions of the maxilla, failure of sublabial incision to heal after Caldwell-luc antrostomy, multiple and extensive fractures of the facial region, Osteomyelitis of the maxilla, injudicious use of instruments during oral procedures, malignancy of the maxillary sinus, Syphilis, malignant granuloma, radiotherapy, implant denture, removal of a large cyst or resection of large tumour involving maxilla, development of tumour causing bone destruction and loosening of teeth.
All the teeth are normal size but appear smaller relative to enlarged jaws. Relative generalized microdontia may be the result of inheritance of a large jaw from one parent, and normal sized teeth from the other.
Nasal dysplasia or nasoschisis is caused by a development arrest of the lateral side of the nose, resulting in a cleft in one of the nasal halves. The nasal septum and cavity can be involved, though this is rare. Nasoschisis is also characterized by hypertelorism.
All the teeth are smaller than the normal size. True generalized microdontia is very rare, and occurs in pituitary dwarfism. Due to decreased levels of growth hormone the teeth fail to develop to a normal size.
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).
Nasomaxillary dysplasia is caused by a development arrest at the junction of the lateral side of the nose and the maxilla, which results in a complete or non-complete cleft between the nose and the orbital floor (nasoocular cleft) or between the mouth, nose and the orbital floor (oronasal-ocular cleft). The development of the lip is normal.
Midfacial malformations can be subdivided into two different groups. One group with hypertelorism, this includes FND. The other with hypotelorism (a decreased distance between the eyes), this includes holoprosencephaly (failure of development of the forebrain). In addition, a facial cleft can be classified using the Tessier classification. Each of the clefts is numbered from 0 to 14. The 15 different types of clefts are then subdivided into 4 groups, based on their anatomical position in the face: midline clefts, paramedian clefts, orbital clefts and lateral clefts. FND is a midline cleft, classified as Tessier 0/14.
Besides this, the additional anomalies seen in FND can be subdivided by region. None of these anomalies are specific for the syndrome of FND, but they do occur more often in patients with FND than in the population. The anomalies that may be present are:
- Nasal: mild anomalies to nostrils that are far apart and a broad nasal root, a notch or cleft of the nose and accessory nasal tags.
- Ocular: narrowed eye slits, almond shaped eyes, epicanthal folds (extra eyelid tissue), epibulbar dermoids (benign tumors of the eye), upper eyelid colombas (full thickness upper eyelid defects), microphtalmos (one or two small eyes), congenital cataract and degeneration of the eye with retinal detachment.
- Facial: telecanthus (an increased distance between the corners of the eye), a median cleft of the upper lip and/or palatum, and a V-shaped hairline.
- Others: polydactyly (an excess of fingers or toes), syndactyly (fused fingers or toes), brachydactyly (short fingers and/or toes), clinodactyly (bending of the fifth fingers towards the fourth fingers), preauricular skin tags, an absent tragus, low set ears, deafness, small frontal sinuses, mental retardation, encephalocele (protrusion of the brain), spina bifida (split spine), meningoencephalocele (protrusion of both meninges), umbilical hernia, cryptorchidism (absence of one or two testes) and possibly cardiac anomalies.
The clefts of the face that are present in FND are vertical clefts. These can differ in severity. When they are less severe, they often present with hypertelorism and normal brain development.
Mental retardation is more likely when the hypertelorism is more severe or when extracephalic anomalies occur.
Binder's Syndrome/Binder Syndrome (Maxillo-Nasal Dysplasia) is a developmental disorder primarily affecting the anterior part of the maxilla and nasal complex (nose and jaw). It is a rare disorder and the causes are unclear.
The characteristics of the syndrome are typically visible. The syndrome involves hypoplasia of variable severity of cartilaginous nasal septum and premaxilla. It includes complete total absence of the anterior nasal spine. There are also associated anomalies of muscle insertions of the upper lip and the nasal floor and of the cervical spine. Affected individuals typically have an unusually flat, underdeveloped midface (midfacial hypoplasia), with an abnormally short nose and flat nasal bridge. They have an underdeveloped upper jaw, relatively protruding lower jaw with anterior mandibular vertical excess and a Class III skeletal and dental (reverse overjet) profile. They have a small frontal sinus and global facial imbalance.
Treatment is encouraged as early as possible with posteroanterior traction on the maxilla and, at about age 8, reinsertion of the nasolabial muscles onto the anterior border of the cartilaginous system. Many who have a severe case of the disorder undergo plastic surgery or orthodontic treatment for cosmetic reasons.
Macrognathism is the condition of abnormally large jaws. It is also called "megagnathia" (antonym: micrognathia).
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 Pai Syndrome is a rare subtype of frontonasal dysplasia. It is a triad of developmental defects of the face, comprising midline cleft of the upper lip, nasal and facial skin polyps and central nervous system lipomas. When all the cases are compared, a difference in severity of the midline cleft of the upper lip can be seen. The mild form presents with just a gap between the upper teeth. The severe group presents with a complete cleft of the upper lip and alveolar ridge.
Nervous system lipomas are rare congenital benign tumors of the central nervous system, mostly located in the medial line and especially in the corpus callosum. Generally, patients with these lipomas present with strokes. However, patients with the Pai syndrome don’t. That is why it is suggested that isolated nervous system lipomas have a different embryological origin than the lipomas present in the Pai syndrome. The treatment of CNS lipomas mainly consists of observation and follow up.
Skin lipomas occur relatively often in the normal population. However, facial and nasal lipomas are rare, especially in childhood. However, the Pai syndrome often present with facial and nasal polyps. These skin lipomas are benign, and are therefore more a cosmetic problem than a functional problem.
The skin lipomas can develop on different parts of the face. The most common place is the nose. Other common places are the forehead, the conjunctivae and the frenulum linguae. The amount of skin lipomas is not related to the severity of the midline clefting.
Patients with the Pai syndrome have a normal neuropsychological development.
Until today there is no known cause for the Pai syndrome.
The large variety in phenotypes make the Pai syndrome difficult to diagnose. Thus the incidence of Pai syndrome seems to be underestimated.
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.
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
Periapical cysts begin as asymptomatic and progress slowly. Subsequent infection of the cyst causes swelling and pain. Initially, the cyst swells to a round hard protrusion, but later on the body resorbs some of the cyst wall, leaving a softer accumulation of fluid underneath the mucous membrane.
Larger cysts may cause bone expansion or displace roots. Discoloration of the affected tooth may also occur. Patient will present negative results to electric and ice test of the affected tooth but will be sensitive to percussion. Surrounding gingival tissue may experience lymphadenopathy. The alveolar plate may exhibit crepitus when palpated.
Periapical cysts exist in two structurally distinct classes:
Periapical true cysts - cysts containing cavities entirely surrounded in epithelial lining. Resolution of this type of cyst requires surgical treatment such as a cystectomy.
Periapical pocket cysts - epithelium lined cavities that have an opening to the root canal of the affected tooth. Resolution may occur after traditional root canal therapy.
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.
Periapical cysts comprise approximately 75% of the types of cysts found in the oral region. The ratio of individuals diagnosed with periapical cysts is 3:2 male to female, as well as individuals between 20 and 60 years old. Periapical cysts occur worldwide.
Types of Periapical cysts:
Apical: 70%
Lateral: 20%
Residual: 10%
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.
In dentistry, a furcation defect is bone loss, usually a result of periodontal disease, affecting the base of the root trunk of a tooth where two or more roots meet ("bifurcation" or "trifurcation"). The extent and configuration of the defect are factors in both diagnosis and treatment planning.
A tooth with a furcation defect typically possessed a more diminished prognosis owing to the difficulty of rendering the furcation area free from periodontal pathogens. For this reason, surgical periodontal treatment may be considered to either close the furcation defect with grafting procedures or allow greater access to the furcation defect for improved oral hygiene.
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)
On physical exam, the fracture appears as a loss of cheek projection with increased width of the face. In most cases, there is loss of sensation in the cheek and upper lip due to infraorbital nerve injury. Facial bruising, periorbital ecchymosis, soft tissue gas, swelling, trismus, altered mastication, diplopia, and ophthalmoplegia are other indirect features of the injury. The zygomatic arch usually fractures at its weakest point, 1.5 cm behind the zygomaticotemporal suture.
If Turner's hypoplasia is found on a canine or a premolar, the most likely cause is an infection that was present when the primary (baby) tooth was still in the mouth. Most likely, the primary tooth was heavily decayed and an area of inflamed tissues around the root of the tooth (called a periapical inflammation), affecting the development of the permanent tooth. The tooth most likely affected by this cause is the canine tooth. The appearance of the abnormality will depend on the severity and longevity of the infection.
If Turner's hypoplasia is found in the front (anterior) area of the mouth, the most likely cause is a traumatic injury to a primary tooth. The traumatized tooth, which is usually a maxillary central incisor, is pushed into the developing tooth underneath it and consequently affects the formation of enamel. Because of the location of the permanent tooth's developing tooth bud in relation to the primary tooth, the most likely affected area on the permanent tooth is the facial surface (the side closer to the lips or cheek). White or yellow discoloration may accompany Turner's hypoplasia. Enamel hypoplasia may also be present.
Turner's hypoplasia usually affects the tooth enamel if the trauma occurs prior to the third year of life. Injuries occurring after this time are less likely to cause enamel defects since the enamel is already calcified.
The same type of injury is also associated with the dilaceration of a tooth.
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.
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.