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

There are no treatment to return to its normal functions. However, there are treatments for the different symptoms.

For the Developmental symptoms, Educational intervention and speech therapy beginning in infancy could help to reduce the high risk for motor, cognitive, speech, and language delay

For theSkeletal features, referral to an orthopedist for consideration of surgical release of contractures. In addition,early referral to physical therapy could help increase joint mobility.

Lastly, Thyroid hormone replacement could help out the thyroid dysfunction

The cause of Primrose syndrome is currently unknown. This condition is extremely rare and seems to spontaneously occur, regardless of family history.

In the case studied by Dalai et al. in 2010, it was found that an abnormally high amount of calcitonin, a hormone secreted by the thyroid gland to stabilize blood calcium levels, was present in the blood serum. This suggests that the thyroid gland is releasing an abnormal amount of calcitonin, resulting in the disruption of calcium level homeostasis. No molecular cause was found, but an expanded microarray analysis of the patient found a 225.5 kb deletion on chromosome 11p between rs12275693 and rs1442927. Whether or not this deletion is related to the syndrome or is a harmless mutation is unknown. The deletion was not present in the patient's mother's DNA sample, but the father's DNA was unavailable.

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

Urofacial (Ochoa) syndrome received the Ochoa name because of the first person to describe it back in 1987, Bernardo Ochoa.

Many of the congenital malformations found with Malpuech syndrome can be corrected surgically. These include cleft lip and palate, omphalocele, urogenital and craniofacial abnormalities, skeletal deformities such as a caudal appendage or scoliosis, and hernias of the umbillicus. The primary area of concern for these procedures applied to a neonate with congenital disorders including Malpuech syndrome regards the logistics of anesthesia. Methods like tracheal intubation for management of the airway during general anesthesia can be hampered by the even smaller, or maldeveloped mouth of the infant. For regional anesthesia, methods like spinal blocking are more difficult where scoliosis is present. In a 2010 report by Kiernan et al., a four-year-old girl with Malpuech syndrome was being prepared for an unrelated tonsillectomy and adenoidectomy. While undergoing intubation, insertion of a laryngoscope, needed to identify the airway for the placement of the endotracheal tube, was made troublesome by the presence of micrognathia attributed to the syndrome. After replacement with a laryngoscope of adjusted size, intubation proceeded normally. Successful general anesthesia followed.

A rare follow-up of a male with Malpuech syndrome was presented by Priolo et al. (2007). Born at term from an uneventful pregnancy and delivery, the infant underwent a surgical repair of a cleft lip and palate. No problems were reported with the procedure. A heart abnormality, atrial septal defect, was also apparent but required no intervention. At age three years, mental retardation, hyperactivity and obsessive compulsive disorder were diagnosed; hearing impairment was diagnosed at age six, managed with the use of hearing aids. Over the course of the decade that followed, a number of psychiatric evaluations were performed. At age 14, he exhibited a fear of physical contact; at age 15, he experienced a severe psychotic episode, characterized by agitation and a loss of sociosexual inhibition. This array of symptoms were treated pharmocologically (with prescription medications). He maintained a low level of mental deficiency by age 17, with moments of compulsive echolalia.

Treatment can include amoxicillin-clavulanic acid, intravenous fluid administration and paracetamol oral for pain relief. Other treatment varies based on the condition and extent of uropathy.

Several studies have reported that life expectancy appears to be normal for people with CCD.

Singleton Merten Syndrome is an autosomal dominate genetic disorder with variable expression with an onset of symptoms during childhood.

The lateral meningocele syndrome is a very rare skeletal disorder with facial anomalies, hypotonia and meningocele-related neurologic dysfunction.

Primrose syndrome is a rare, slowly progressive genetic disorder that can vary symptomatically between individual cases, but is generally characterised by ossification of the external ears, learning difficulties, and facial abnormalities. It was first described in 1982 in Scotland's Royal National Larbert Institution by Dr D.A.A. Primrose.

Primrose syndrome appears to occur spontaneously, regardless of family history. The cause is currently unknown and there are no known treatments.

Around 5 years of age, surgical correction may be necessary to prevent any worsening of the deformity. If the mother has dysplasia, caesarian delivery may be necessary. Craniofacial surgery may be necessary to correct skull defects. Coxa vara is treated by corrective femoral osteotomies. If there is brachial plexus irritation with pain and numbness, excision of the clavicular fragments can be performed to decompress it. In case of open fontanelle, appropriate headgear may be advised by the orthopedist for protection from injury.

This syndrome was first described by Lehman et al. in 1977. This paper described a 14-year-old girl with a number of unusual findings. Her mother shared some of the same findings. Since then over a dozen additional cases have been reported.

In 1988, Goldblatt et al. first reported a 4-year-old boy with hypoplastic patellae, mental retardation, scrotal hypoplasia, skeletal deformities, renal anomalies, flattened nasal bridge, and short stature. Later in 2000, Cormier-Daire et al. reported seven patients with genital anomalies (scrotal hypoplasia and cryptorchidism in the boys and clitoral hypertrophy in the girls), facial dysmorphism, renal anomalies, absent patella, and severe mental retardation in the two survivors. The condition is now known as genitopatellar syndrome.

Seaver Cassidy syndrome is a very rare disorder characterized by certain facial, genital, and skeletal deformities, as well as an unusual susceptibility to bleeding. Seaver Cassidy syndrome was first described in 1991 by Laurie Seaver and Suzanne Cassidy.

Nablus mask-like facial syndrome is a microdeletion syndrome triggered by a deletion at chromosome 8 q22.1 that causes a mask-like facial appearance in those affected.

It is characterized by a narrowing of the eyes, tight, glistening facial skin, and a flat, broad nose. Other features of the syndrome include malformed ears, unusual hair patterns on the scalp, bent fingers and toes and joint deformities in the hands and feet, unusual teeth, mild developmental delay, cryptorchidism, and a generally happy disposition. It is a rare genetic disorder by inheritance found in Palestinian people named after Nablus city in the West Bank. It is part of many new genetic disorders of newborns that is increasing exponentially in Arabs in recent years as reported by Centre for Arab Genomic Studies in Dubai.

French doctors Weismann-Netter and Stuhl characterized the features of this disorder in their report first describing the association in seven patients in 1954. They believed these seven patients had mistakenly been diagnosed as congenital syphilis or rickets, which remain the primary considerations in the differential diagnosis of this syndrome today.

Franceschetti–Klein syndrome (also known as "Mandibulofacial dysostosis") is a syndrome that includes palpebral antimongoloid fissures, hypoplasia of the facial bones, macrostomia, vaulted palate, malformations of both the external and internal ear, buccal-auricular fistula, abnormal development of the neck with stretching of the cheeks, accessory facial fissures, and skeletal deformities.

It is sometimes equated with Treacher Collins syndrome.

Weismann-Netter-Stuhl syndrome, also known as Weismann-Netter Syndrome or more technically by the term tibioperoneal diaphyseal toxopachyosteosis, is a rare disorder characterized by bowing of the lower legs and an abnormal thickening of thinner bone in the leg.

The main sign is anterior bowing and posterior cortical thickening of the diaphyses of both the tibiae and fibulae. It is thought to be inherited in an autosomal dominant fashion, and is most often bilateral and symmetric in nature. Associated features include dwarfism and mild intellectual disability, as well as a process known as tibialization of the fibulae, which involves thickening and enlargement of these bones to an extent resembling the tibiae. The combination of the presence of tibialization of the fibulae, which is highly specific for the disorder, and the absence of laboratory abnormalities ruling out alternative diagnoses including rickets, essentially confirms the diagnosis.

Branchio-oculo-facial syndrome (BOFS) is a disease that arises from a mutation in the TFAP2A gene. It is a rare autosomal dominant disorder that starts to affect a child's development before birth. Symptoms of this condition include skin abnormalities on the neck, deformities of the ears and eyes, and other distinctive facial features such a cleft lip along with slow growth, mental retardation and premature graying of hair.

One dental textbook defines it as: “Dollicofacial, there is excess of lower facial height usually associated with lower occlusal and mandibular plane angles.” This is often associated “with vertical maxillary excess and mandibular hypoplasia.” Luc P. M. Tourne, a Fellow in the Department of TMJ and Craniofacial Pain at the University of Minnesota School of Dentistry, noted: "There is a clinically recognizable facial morphology, the long face syndrome, which has been incompletely described in the literature," However, her study of 31 adults with this syndrome, which included "analysis of esthetics, skeletal morphology, and occlusion" confirmed "this basic dentofacial deformity" has associations " with excessive vertical growth of the maxilla." She reported that closed bite and dental open are two pf the syndrome's variants.

The treatment for young patients troubled by long face syndrome is to halt and control descent of the lower jaw and to prevent the eruption of posterior teeth. In severe cases of deformity, a mixture of orthodontics and orthognathic surgery may be the only effective solution. The long term (more than 6 years) effectiveness of surgical treatments for long face syndrome has been subject to study.

"In the American literature, the terms long-face syndrome and short-face syndrome are often used." To be sure, there are reported "long and the short face anomalies" and open bite cases. However, in the opinion of Hugo Obwegeser, there is no medical justification for naming theme as a "syndrome" the signs and symptoms do not meet the definitional threshold.

There is controversy concerning the use of the descriptor "long-face syndrome." While increased anterior "total and lower face height" in many ages, combined with vertical maxillary excess in adults has been observed, the causes are controversial. Specifically, there is disagreement about possible potential environmental influences on genetic components.

Anecdotally, it was said to be a genetic condition, which could only be corrected with “massive amounts” of debilitating, frequent and long dental and facial reconstructive surgery.

For children, there is a concern that mouth breathing can contribute to the development of long face syndrome. A recent study finds that it is a growing problem which should be treated as "It won't just go away." In addition to mouth breathing, it may be associated with sleep apnea.

Because of Long face syndrome's sometime association with pediatric obstructive sleep apnea (OSA) and allergic reactions, it is essential that treating physicians differentiate the conditions and the treatments; treating one may not cure the other. Multilevel coblation surgery is sometimes used to correct moderate to severe OSA, and Long Face Syndrome can be a rare factor in considering surgery.

ICF syndrome (or Immunodeficiency, Centromere instability and Facial anomalies syndrome) is a very rare autosomal recessive immune disorder.

It was estimated that only about 50 cases of BOFS have been documented in the medical literature as of 2004.

Most patients with hyper IgE syndrome are treated with long-term antibiotic therapy to prevent staphylococcal infections. Good skin care is also important in patients with hyper IgE syndrome. High-dose intravenous gamma-globulin has also been suggested for the treatment of severe eczema in patients with HIES and atopic dermatitis.

Malpuech facial clefting syndrome, also called Malpuech syndrome or Gypsy type facial clefting syndrome, is a rare congenital syndrome. It is characterized by facial clefting (any type of cleft in the bones and tissues of the face, including a cleft lip and palate), a appendage (a "human tail"), growth deficiency, intellectual and developmental disability, and abnormalities of the renal system (kidneys) and the male genitalia. Abnormalities of the heart, and other skeletal malformations may also be present. The syndrome was initially described by Guilliaume Malpuech and associates in 1983. It is thought to be genetically related to Juberg-Hayward syndrome. Malpuech syndrome has also been considered as part of a spectrum of congenital genetic disorders associated with similar facial, urogenital and skeletal anomalies. Termed "3MC syndrome", this proposed spectrum includes Malpuech, Michels and Mingarelli-Carnevale (OSA) syndromes. Mutations in the "COLLEC11" and "MASP1" genes are believed to be a cause of these syndromes. The incidence of Malpuech syndrome is unknown. The pattern of inheritance is autosomal recessive, which means a defective (mutated) gene associated with the syndrome is located on an autosome, and the syndrome occurs when two copies of this defective gene are inherited.