The goals of treatment in infants with Robin sequence focus upon breathing and feeding, and optimizing growth and nutrition despite the predisposition for breathing difficulties. If there is evidence of airway obstruction (snorty breathing, apnea, difficulty taking a breath, or drops in oxygen), then the infant should be placed in the sidelying or prone position, which helps bring the tongue base forward in many children. One study of 60 infants with PRS found that 63% of infants responded to prone positioning (Smith and Senders, 2006, Int J Pediatr Oto). 53% of the infants in this study required some form of feeding assistance, either nasogastric tube or gastrostomy tube feedings (feeding directly into the stomach). In a separate study of 115 children with the clinical diagnosis of PRS managed at 2 different hospitals in Boston (Evans et al., 2006, In J Pediatr Oto), respiratory distress was managed successfully in 56% without an operation (either by prone positioning, short term intubation, or placement of a nasopharyngeal airway). In this study, gastrostomy tube feeding were placed in 42% of these infants due to feeding difficulties.

Gastroesophageal reflux (GERD) seems to be more prevalent in children with Robin sequence (Dudkiewicz, March 2000, CPCJ). Because reflux of acidic contents in the posterior pharynx and upper airway can intensify the symptoms of Robin sequence, specifically by worsening airway obstruction, it is important to maximize treatment for GER in children with PRS and reflux symptoms. Treatment may include upright positioning on a wedge (a tucker sling may be needed if the baby is in the prone position), small and frequent feedings (to minimize vomiting), and/or pharmacotherapy (such as proton pump inhibitors).

In nasopharyngeal cannulation (or placement of the nasopharyngeal airway or tube), the infant is fitted with a blunt-tipped length of surgical tubing (or an endotracheal tube fitted to the child), which is placed under direct visualization with a laryngoscope, being inserted into the nose and down the pharynx (or throat), ending just above the vocal cords. Surgical threads fitted through holes in the outside end of the tube are attached to the cheek with a special skin-like adhesive material called 'stomahesive', which is also wrapped around the outside end of the tube (but not over the opening at the end) to keep the tube in place. This tube or cannula, which itself acts as an airway, primarily acts as a sort of "splint" which maintains patency of the airway by keeping the tongue form falling back on the posterior pharyngeal wall and occluding the airway, therefore preventing airway obstruction, hypoxia and asphyxia. Nasopharyngeal airways are not available at every center, however, when available, nasopharyngeal cannulation should be favored over the other treatments mentioned in this article, as it is far less invasive; it allows the infant to feed without the further placement of a nasogastric tube. This treatment may be utilized for multiple months, until the jaw has grown enough so that the tongue assumes a more normal position in the mouth and airway (at birth, the jaws of some infants are so underdeveloped that only the tip of the tongue can be seen when viewed in the throat). Some institutions discharge the infant home with a nasopharyngeal tube in place (Citation: KD Anderson, May 2007, CPCJ).

Distraction osteogenesis (DO), also called a "Mandibular Distraction", can be used to correct abnormal smallness of one or both jaws seen in patients with Robin Sequence. Enlargement of the lower jaw brings the tongue forward, preventing it from obstructing the upper airway. The process of DO begins with preoperative assessment. Doctors use three-dimensional imaging to identify the parts of the patient's facial skeleton that need repositioning and determine the magnitude and direction of distraction. They may then select the most appropriate distraction device or sometimes have custom devises fabricated. When possible, intraoral devices are used.

DO surgery starts with an osteotomy (surgical division or sectioning of bone) followed by the distraction device being placed under the skin and across the osteotomy. A few days later, the two ends of the bone are very gradually pulled apart through continual adjustments that are made to the device by the parents at home. The adjustments are made by turning a small screw that protrudes through the skin, usually at a rate of 1 mm per day. This gradual distraction leads to formation of new bone between the two ends. After the process is complete, the osteotomy is allowed to heal over a period of six to eight weeks. A small second surgery is then performed to remove the device.

The cleft palate is generally repaired between the ages of 6½ months and 2 years by a plastic or maxillofacial surgeon. In many centres there is now a cleft lip and palate team comprising both of these specialties, as well as a coordinator, a speech and language therapist, an orthodontist, sometimes a psychologist or other mental health specialist, an audiologist, an otorhinolaryngologist (ENT surgeon) and nursing staff. The glossoptosis and micrognathism generally do not require surgery, as they improve to some extent unaided, though the mandibular arch remains significantly smaller than average. In some cases jaw distraction is needed to aid in breathing and feeding. Lip-tongue attachment is performed in some centres, though its efficacy has been recently questioned.

The prevalence has been estimated at 1 in 10,000 births, but exact values are hard to know because some that have the symptoms rarely have Pierre-Robin sequence (without any other associated malformation).

There is no known specific treatment for this condition. Management is supportive.

Many professionals that are likely to be involved in the treatment of those with Stickler's syndrome, include anesthesiologists, oral and maxillofacial surgeons; craniofacial surgeons; ear, nose, and throat specialists, ophthalmologists, optometrists, audiologists, speech pathologists, physical therapists and rheumatologists.

While not always pathological, it can present as a birth defect in multiple syndromes including:

- Catel–Manzke syndrome

- Bloom syndrome

- Coffin–Lowry syndrome

- congenital rubella

- Cri du chat syndrome

- DiGeorge's syndrome

- Ehlers-Danlos syndrome

- fetal alcohol syndrome

- Hallermann-Streiff syndrome

- Hemifacial microsomia (as part of Goldenhar syndrome)

- Juvenile idiopathic arthritis

- Marfan syndrome

- Noonan syndrome

- Pierre Robin syndrome

- Prader–Willi syndrome

- Progeria

- Russell-Silver syndrome

- Seckel syndrome

- Smith-Lemli-Opitz syndrome

- Treacher Collins syndrome

- Trisomy 13 (Patau syndrome)

- Trisomy 18 (Edwards syndrome)

- Wolf–Hirschhorn syndrome

- X0 syndrome (Turner syndrome)

There is no medical treatment for either syndrome but there are some recommendations that can help with prevention or early identification of some of the problems. Children with either syndrome should have their hearing tested, and adults should be aware that the hearing loss may not develop until the adult years. Yearly visits to an ophthalmologist or other eye care professional who has been informed of the diagnosis of Stickler or Marshall syndrome is important for all affected individuals. Children should have the opportunity to have myopia corrected as early as possible, and treatment for cataracts or detached retinas may be more effective with early identification. Support for the joints is especially important during sports, and some recommend that contact sports should be avoided by those who have very loose joints.

While there is no specific treatment for the underlying genetic cause of LFS; corrective procedures, preventive intervention measures and therapies may be considered in the treatment and management of the many craniofacial, orthopedic and psychiatric problems associated with the disorder. More pressing issues such as cardiac involvement or epileptic seizures should be routinely examined and monitored. Close attention and specialized follow-up care, including neuropshycological evaluation methods and therapies, and special education, should be given to diagnose and prevent psychiatric disorders and related behavioral problems such as psychosis and outbursts of aggression.

Currently there are only around 26 people in the world that are known to have this rare condition. Inheritance is thought to be X-linked recessive.

Catel–Manzke syndrome is a rare genetic disorder characterized by distinctive abnormalities of the index fingers; the classic features of Pierre Robin syndrome; occasionally with additional physical findings. "Pierre Robin syndrome" refers to a sequence of abnormalities that may occur as a distinct syndrome or as part of another underlying disorder. Pierre Robin syndrome is characterized by an unusually small jaw (micrognathia), downward displacement or retraction of the tongue (glossoptosis), and incomplete closure of the roof of the mouth (cleft palate). It is also linked to hyper mobility syndrome.

There is no cure as of now. Treatment is directed towards the specific symptoms that are present in each individual. Individuals with hearing loss are able to get treated with hearing aids.

Lujan–Fryns syndrome is a rare X-linked dominant syndrome, and is therefore more common in males than females. Its prevalence within the general population has not yet been determined.

It can be detected by the naked eye as well as dental or skull X-Ray testing.

There is currently no treatment or cure for Waardenburg syndrome. The symptom most likely to be of practical importance is deafness, and this is treated as any other irreversible deafness would be. In marked cases there may be cosmetic issues. Other abnormalities (neurological, structural, Hirschsprung disease) associated with the syndrome are treated symptomatically.

The cause of this condition is not known. A genetic basis is suspected. More than one case have been reported in three families.

Glossoptosis is a medical condition and abnormality which involves the downward displacement or retraction of the tongue. It may cause non-fusion of the hard palate causing cleft palate.

It is one of the features of Pierre Robin sequence and Down syndrome.

Currently, research is focusing on identifying the role of the genes on 18q in causing the signs and symptoms associated with proximal deletions of 18q.

Nager syndrome is thought to be caused by haploinsufficiency of the spliceosomal factor SF3B4.

Nager acrofacial dysostosis is a genetic congenital anomaly syndrome. Nager syndrome displays several or all of the following characteristics: underdevelopment of the cheek and jaw area, down-sloping of the opening of the eyes, lack or absence of the lower eyelashes, kidney or stomach reflux, hammer toes, shortened soft palate, lack of development of the internal and external ear, possible cleft palate, underdevelopment or absence of the thumb, hearing loss (see hearing loss with craniofacial syndromes) and shortened forearms, as well as poor movement in the elbow, and may be characterized by accessory tragi. Occasionally, affected individuals develop vertebral anomalies such as scoliosis. The inheritance pattern is said to be autosomal but there are arguments as to whether it is autosomal dominant or autosomal recessive. Most cases tend to be sporadic. Nager syndrome is also linked to five other similar syndromes: Miller syndrome, Treacher Collins, Pierre Robin, Genee-Wiedemann, and Franceschetti-Zwahlen-Klein.

At present, treatment for proximal 18q- is symptomatic, meaning that the focus is on treating the signs and symptoms of the condition as they arise.

First arch syndromes are congenital defects caused by a failure of neural crest cells to migrate into the first pharyngeal arch. They can produce facial anomalies. Examples of first arch syndromes include Treacher Collins syndrome and Pierre Robin syndrome.

Weissenbacher-Zweymüller syndrome affects males and females in the same numbers. About 30 cases have been reported in medical literature. This disorder can be underdiagnosed causing no true frequency in the population. Only 30 cases have been reported in medical literature.

Overall, the estimated prevalence of Stickler syndrome is about 1 in 10,000 people. Stickler syndrome affects 1 in 7,500 to 9,000 newborns.

The overall incidence is ~1/42,000 to 1/50,000 people. Types I and II are the most common types of the syndrome, whereas types III and IV are rare. Type 4 is also known as Waardenburg‐Shah syndrome (association of Waardenburg syndrome with Hirschsprung disease).

Type 4 is rare with only 48 cases reported up to 2002.

About 1 in 30 students in schools for the deaf have Waardenburg syndrome. All races and sexes are affected equally. The highly variable presentation of the syndrome makes it difficult to arrive at precise figures for its prevalence.

Marshall syndrome is a genetic disorder of the connective tissue which can cause hearing loss. The three most common areas to be affected are the eyes which are uncommonly large, joints and the mouth and facial structures. Marshall syndrome and Stickler syndrome closely resemble each other; in fact they are so similar, some say they are the same.

Natal teeth are teeth that are present above the gumline (have already erupted) at birth, and neonatal teeth are teeth that emerge through the gingiva during the first month of life (the neonatal period).

The incidence of neonatal teeth varies considerably, between 1:700 and 1:30,000 depending on the type of study; the highest prevalence is found in the only study that relies on personal examination of patients.