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Cleft lip ( cheiloschisis ) and cleft palate ( palatoschisis ) (colloquially known as harelip ), which can also occur together as cleft lip and palate , are variations of a type of clefting congenital deformity caused by abnormal facial development during gestation. A cleft is a fissure or opening—a gap. It is the non-fusion of the body's natural structures that form before birth. Approximately 1 in 700 children born have a cleft lip and/or a cleft palate.
Clefts can also affect other parts of the face, such as the eyes, ears, nose, cheeks, and forehead. In 1976, Paul Tessier described fifteen lines of cleft. Most of these craniofacial clefts are even more rare and are frequently described as Tessier clefts using the numerical locator devised by Tessier.
A cleft lip or palate can be successfully treated with surgery, especially so if conducted soon after birth or in early childhood.
Cleft lip and palate
If the cleft does not affect the palate structure of the mouth it is referred to as cleft lip. Cleft lip is formed in the top of the lip as either a small gap or an indentation in the lip (partial or incomplete cleft) or it continues into the nose (complete cleft). Lip cleft can occur as a one sided (unilateral) or two sided (bilateral). It is due to the failure of fusion of the maxillary and medial nasal processes (formation of the primary palate).
A mild form of a cleft lip is a microform cleft . A microform cleft can appear as small as a little dent in the red part of the lip or look like a scar from the lip up to the nostril. In some cases muscle tissue in the lip underneath the scar is affected and might require reconstructive surgery. It is advised to have newborn infants with a microform cleft checked with a craniofacial team as soon as possible to determine the severity of the cleft.
Cleft palate
Cleft palate is a condition in which the two plates of the skull that form the hard palate (roof of the mouth) are not completely joined. The soft palate is in these cases cleft as well. In most cases, cleft lip is also present. Cleft palate occurs in about one in 700 live births worldwide.
Palate cleft can occur as complete (soft and hard palate, possibly including a gap in the jaw) or incomplete (a 'hole' in the roof of the mouth, usually as a cleft soft palate). When cleft palate occurs, the uvula is usually split. It occurs due to the failure of fusion of the lateral palatine processes, the nasal septum, and/or the median palatine processes (formation of the secondary palate).
The hole in the roof of the mouth caused by a cleft connects the mouth directly to the nasal cavity.
Note: the next images show the roof of the mouth. The top shows the nose, the lips are colored pink. For clarity the images depict a toothless infant.
A direct result of an open connection between the oral cavity and nasal cavity is velopharyngeal inadequacy (VPI). Because of the gap, air leaks into the nasal cavity resulting in a hypernasal voice resonance and nasal emissions. Secondary effects of VPI include speech articulation errors (e.g., distortions, substitutions, and omissions) and compensatory misarticulations (e.g., glottal stops and posterior nasal fricatives).. Possible treatment options include speech therapy, prosthetics, augmentation of the posterior pharyngeal wall, lengthening of the palate, and surgical procedures.
Submucous cleft palate (SMCP) can also occur, which is an occult cleft of the soft palate with a classic clinical triad of bifid uvula, a furrow along the midline of the soft palate, and a notch in the posterior margin of the hard palate.
Prevalence among ethnic groups
Main article: Clefting prevalence in different culturesPrevalence rates reported for live births for Cleft lip with or without Cleft Palate (CL +/- P) and Cleft Palate alone (CPO) varies within different ethnic groups.
The highest prevalence rates for (CL +/- P) are reported for Native Americans and Asians. Africans have the lowest prevalence rates.
- Native Americans: 3.74/1000
- Japanese: 0.82/1000 to 3.36/1000
- Chinese: 1.45/1000 to 4.04/1000
- Caucasians: 1.43/1000 to 1.86/1000
- Latin Americans: 1.04/1000
- Africans: 0.18/1000 to 1.67/1000
Rate of occurrence of CPO is similar for Caucasians, Africans, North American natives, Japanese and Chinese. The trait is dominant.
Prevalence of "cleft uvula" has varied from .02% to 18.8% with the highest numbers found among Chippewa and Navajo and the lowest generally in Africans.
Causes of cleft
The development of the face is coordinated by complex morphogenetic events and rapid proliferative expansion, and is thus highly susceptible to environmental and genetic factors, rationalising the high incidence of facial malformations. During the first six to eight weeks of pregnancy, the shape of the embryo's head is formed. Five primitive tissue lobes grow:
If these tissues fail to meet, a gap appears where the tissues should have joined (fused). This may happen in any single joining site, or simultaneously in several or all of them. The resulting birth defect reflects the locations and severity of individual fusion failures (e.g., from a small lip or palate fissure up to a completely malformed face).
The upper lip is formed earlier than the palate, from the first three lobes named a to c above. Formation of the palate is the last step in joining the five embryonic facial lobes, and involves the back portions of the lobes b and c. These back portions are called palatal shelves, which grow towards each other until they fuse in the middle. This process is very vulnerable to multiple toxic substances, environmental pollutants, and nutritional imbalance. The biologic mechanisms of mutual recognition of the two cabinets, and the way they are glued together, are quite complex and obscure despite intensive scientific research.
Genetic factors contributing to cleft lip and cleft palate formation have been identified for some syndromic cases, but knowledge about genetic factors that contribute to the more common isolated cases of cleft lip/palate is still patchy.
If a person is born with a cleft, the chances of that person having a child with a cleft, given no other obvious factor, rises to 1 in 14. Many clefts run in families, even though in some cases there does not seem to be an identifiable syndrome present, possibly because of the current incomplete genetic understanding of midfacial development.
Environmental influences may also cause, or interact with genetics to produce, orofacial clefting. An example for how environmental factors might be linked to genetics comes from research on mutations in the gene PHF8 that cause cleft lip/palate (see above). It was found that PHF8 encodes for a histone lysine demethylase, and is involved in epigenetic regulation. The catalytic activity of PHF8 depends on molecular oxygen, a fact considered important with respect to reports on increased incidence of cleft lip/palate in mice that have been exposed to hypoxia early during pregnancy. In humans, fetal cleft lip and other congenital abnormalities have also been linked to maternal hypoxia, as caused by e.g. maternal smoking, maternal alcohol abuse or some forms of maternal hypertension treatment. Other environmental factors that have been studied include: seasonal causes (such as pesticide exposure); maternal diet and vitamin intake; retinoids - which are members of the vitamin A family; anticonvulsant drugs; alcohol; cigarette use; nitrate compounds; organic solvents; parental exposure to lead; and illegal drugs (cocaine, crack cocaine, heroin, etc).
Current research continues to investigate the extent to which Folic acid can reduce the incidence of clefting.
Diagnosis
Traditionally, the diagnosis is made at the time of birth by physical examination. Recent advances in prenatal diagnosis have allowed obstetricians to diagnose facial clefts in utero.
Treatment
Cleft lip and palate is very treatable; however, the kind of treatment depends on the type and severity of the cleft.
Most children with a form of clefting are monitored by a cleft palate team or craniofacial team through young adulthood. Care can be lifelong. Treatment procedures can vary between craniofacial teams. For example, some teams wait on jaw correction until the child is aged 10 to 12 (argument: growth is less influential as deciduous teeth are replaced by permanent teeth, thus saving the child from repeated corrective surgeries), while other teams correct the jaw earlier (argument: less speech therapy is needed than at a later age when speech therapy becomes harder). Within teams, treatment can differ between individual cases depending on the type and severity of the cleft.
Cleft lip treatment
Within the first 2–3 months after birth, surgery is performed to close the cleft lip. While surgery to repair a cleft lip can be performed soon after birth, the often preferred age is at approximately 10 weeks of age, following the "rule of 10s" coined by surgeons Wilhelmmesen and Musgrave in 1969 (the child is at least 10 weeks of age; weighs at least 10 pounds, and has at least 10g hemoglobin). If the cleft is bilateral and extensive, two surgeries may be require
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