Cleft growth after primary palatoplasy. Factors such

Cleft
palate is among the most common deformities of the craniofacial region, with a
prevalence of clefts being somewhere between 27,000 and 33,000 clefts/year in
India9. The presence of a cleft palate leads to feeding
difficulties, hearing impairment, impaired speech development, and the
possibility of decreased facial growth.

 

Cleft
palate patients develop an impaired midfacial growth after primary palatoplasy.

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Factors
such as intrinsic developmental deficiencies and functional distortions are
initially involved but palatal surgery seems to be a main factor in these growth
problems 10-16. A strong indication for the involvement of iatrogenic factors
is the largely undisturbed maxillary growth in untreated patients 17,18,19.
In treated patients, the healing of surgical wounds after palatoplasty is
probably responsible for the growth disturbances 20.

 

Wound
healing process is quicker in intraoral wounds than in the skin and
produces  less scar tissue. 21.
Decreased  levels of pro-inflammatory and
pro-fibrotic cytokines have been found in mucosal wounds 22. The presence of
saliva and large numbers of bacteria also have an influence on intraoral wound
healing 23. Saliva contains many growth factors such as epidermal growth
factor

(EGF).
Also, phenotypic differences between skin and mucosal fibroblasts may be
involved 24).  In palatal mucosa, the
mucosa and periosteum are merged and attached to the palatal bone 25. The palatal
mucoperiosteum is much more rigid than buccal mucosa and it contains fewer
elastin fiberes26. The palatal mucosal epithelium is generally thicker than  the buccal mucosa. Therefore, the
physiological and mechanical characteristics of the palatal tissue is different
from buccal mucosa, which explains the differences in the outcome of the wound
healing process 27

 

Enlow 28
states that: Growth is not “programmed”
within the calcified part of the bone itself. The “blueprint” for the design,
construction, and growth of a bone lies in the functional matrix: the composite
of the muscles, tongue, lips, cheeks, integument, mucosa, connective tissue,
nerves, blood vessel, airways, pharynx, the brain as an organ mass, tonsils,
adenoids, and so on. Growth fields (growth sites) for example, a suture and the
alveolar bone housing teeth, throughout a bone do not have the

same rate of growth activity. Some
“fields” grow much more rapidly or to a greater extent than others. The same is
true for resorptive fields. All surfaces are sites of growth; relocation of the
bone, going from one location to another, is the basis for remodeling.

 

In the
maxilla, the palatal growth is in the downward direction by periosteal
resorption on the nasal side and
periosteal deposition on the oral side.
The nasal mucosa provides the periosteum on
one side and the oral mucosa provides it on the other side. This results in a
downward location of the  palatal maxillary arch . Depending on the extent of palatal surgery and the resulting scar tissue, the stability of
a region can be disrupted if the
results negatively affect the pattern of resorptive
and depository fields on bone and at the suture;
that is, scarring can work against growth. As the midface grows, bone is laid down in the sutures surrounding
the maxillary complex. Any damage to one
of these sutures can interfere with the direction and amount of growth. For
example, an excessive amount of
scarring at the pterygomaxillary suture, (PTM) or at the premaxillary vomerine
suture (PVS), will interfere with
anteroposterior and vertical maxillary and premaxillary growth.

 

Growth
movement of the premaxilla is produced by the growth expansion of all the bones
behind and

above it
and by growth in other parts of the maxilla, especially at the premaxillary
vomerine suture (PVS). The premaxilla itself contributes a major part of its own
forward growth movement through changes at the PVS. These displacement growth movements
are a result of the “carry effect,” as Enlow calls it, which is produced by the
expansion of the soft tissues associated with the bones, not a “pushing effect”
of bones against bones. Scarring of the palatal mucoperiosteum, therefore, acts
to interfere with the “carry effect,” thus preventing the change in position of
the maxilla within the face.

 

 

In the last
century, surgeons involved in cleft palate treatment usually performed surgical
procedures whose sole purpose was to “close the hole” as early as possible
without considering the ultimate effect of the surgery on palatal, facial, or
speech development. These procedures, Millard 29 reports, fall into three
categories:

1. The use
of various kinds of flaps from other parts of the body to cover the cleft
space.

2.
Treating the edges of the cleft so that they could be sutured together by
pulling the mucoperiosteum

over the
cleft. Failure of a lasting union led to the use of laterally positioned
relaxation incisions by Dieffenback in 1826 and von Langenbeck in 1862 30.

3. Staged
surgical treatment.

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