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doi:10.1016/j.joms.2009.07.099
Report of a Case
Our patient, a 52-year-old woman, sought orthodontic
treatment complaining of unstable occlusion. During anamnesis, the patient reported hypertension, which was under
control, and smoking habits (2 packs per day). Computerbased facial analysis (Dolphin Imaging 10.0TM, Chatsworth,
CA) revealed a retro-positioned maxilla and mandible, along
with Class II malocclusion. Panoramic and intraoral periapical x-ray images suggested the existence of supraosseous
periodontal defects around the maxillary teeth, extending
to the roots of the cervical third.
Orthodontic treatment planning consisted of teeth leveling and alignment associated with orthognathic surgery of
the jaws, comprising single piece advancement of the maxilla and the mandible, as suggested by Arnett et al.14 According to facial and dental cast analysis performed by the
software, a 4-mm advance of the maxilla and 3-mm advance
of the mandible was predicted. No transversal or vertical
alterations were planned. The patient was informed about
1403
PEREIRA ET AL
the risks of complications, and signed a formal consent form
before surgery. In addition, the patient was given a recommendation to stop smoking and was referred to a cardiologist and anesthesiologist for physical examination. Neither
physician detected any systemic alterations that would pose
a life-threatening risk during surgery.
Therefore, Le Fort I and bilateral sagittal split osteotomies
were performed under general anesthesia. After placement
of the maxilla to the planned position, bony interferences
were removed. At this moment, an uncommon bleeding
was noticed in the posterior region of the maxilla, and
proper hemostasis was accomplished by compression with
gauze. DPAs were preserved to maintain blood supply for
the maxilla. Bony segments were fixed by rigid fixation with
plate and screws.
During the first 24-hour postoperative period, the patient
presented moderate and diffuse swelling of the middle third
at both sides, stable occlusion maintained by maxillomandibular fixation, and normal-color mucosa. On the seventh
postoperative day, the occlusion was stable, but the mucosa
overlying the maxilla was ischemic and covered by a
pseudomembrane that could be dislocated by scraping. No
bleeding was noticed after this maneuver. Neither pain nor
discomfort was reported by the patient, who started smoking again on the third postoperative day. The maxillomandibular fixation was removed and generalized marginal tissue recession was observed in the left and right maxillary
teeth. Also, an ulcer in the left side of the hard palate was
noticed (Fig 1). A panoramic x-ray image showed that the
osteosynthesis was properly positioned.
Mouthwash with peroxide, antibiotic therapy (to avoid
secondary infection), cessation of cigarette smoking, and
antihypertensive drug intake were recommended, along
with treatment with hyperbaric oxygenation. No anticoagulants were administered.
A protocol of 20 sessions of hyperbaric oxygenation was
proposed, twice a day during the first week and once a day
during the second week, starting on the eighth postoperative day (Fig 2). After the fourth session of hyperbaric
oxygenation, the patient returned for postoperative examination, with clinical improvement of the labial and gingival
mucosa irrigation and color.
On the eleventh day, mouth washing with peroxide was
suspended because the patient was complaining of a burning sensation after use. The clinical appearance on the
Discussion
This case report describes an unexpected aseptic
necrosis of the maxilla that occurred in a middle-aged
woman who was a heavy smoker. Treatment was
performed with hyperbaric oxygenation, resulting in
1404
advantages of ligating DPAs during surgery are decreased risk of postoperative bleeding, easier maxillary mobilization, and shortening of surgical time.7,21
Hemorrhage has been considered as a major complication in the first 48 postoperative hours, requiring
blood transfusion in 1% to 1.1% of the cases.1,3 However, blood transfusion should be avoided because of
associated morbidity.1,22 Excessive blood loss occurring during surgery or several hours later is mainly
related to maxillary osteotomies. Controlled hypotensive general anesthesia and postpositioning the patient in a slight anti-Trendelenburg position, along
with use of a local anesthetic containing a vasoconstrictor, may help to reduce blood loss.1 However,
when using hypotensive anesthesia, laceration of the
vessels may be masked, and even intraoperative inspection of vessel integrity does not guarantee that no
bleeding will develop afterward.21
Preserving DPA vessels during surgery is justified by
the hypothetical benefit of maintaining blood flow
and decreasing the risk of ischemic complications.21
The known risk is postoperative bleeding caused by
unrecognized laceration of the DPA.9,11,21 A reasonable approach, therefore, is to routinely preserve the
integrity of these vessels when feasible, and to ligate
them when enhanced accessibility or visualization is
required, such as superior or posterior repositioning
of the posterior maxilla, allowing visualization and
access to the tuberosity-pterygoid plate junction, and
facilitating repositioning of the maxilla.8 In clinical
practice, bone contiguous to vessels is routinely removed by careful and meticulous use of a sharp osteotome and Kerrison forceps.9 Vertical movements,
especially setbacks, could perhaps lead to injuries of
the DPA with subsequent thrombosis, even if no rupture is observed.
DPAs can be damaged intraoperatively during
initial osteotomy cuts, maxillary down fracture,
PEREIRA ET AL
1405
GBF during Le Fort I osteotomy. The transosseous and
soft-tissue collateral blood circulation and the freely
anastomosed plexus of the gingiva, vestibule, palate,
nose, maxillary sinus, and periodontium provided the
necessary blood supply after sectioning of the descending palatine vessels.19,20 Although bone segmentation, stretching of the vascular pedicle, flap
design, and bilateral sectioning of the DPA have
been implicated in impairing the hemodynamics of
the maxillary pedicle,6 Bell et al9 showed that vascular alterations are only transient and are compatible with clinical success without resultant ischemic complications. Stretching the vascular pedicle
by a 7- to 10-mm anterior displacement of the maxillary segment did not interfere with eventual osseous healing and revascularization.25
It is not known to what degree, and for how long,
blood flow can be impaired so as not to disturb
continuous blood supply to the tissues, as well as the
range of individual variability. Aseptic necrosis, with
loss of tooth vitality, may occur much more commonly than is clinically apparent after maxillary surgery because obvious clinical signs and symptoms
frequently do not accompany this situation.6 Tooth
vitality tests commonly used in dentistry, involving
either electrical or thermal stimulation, are unreliable
after orthognathic surgery because sensory fibers
from the trigeminal nerve are severed at surgery.
Gingival bleeding is reduced in patients who
smoke, even in the presence of moderate to severe
periodontal disease, accompanied by reduction of
other clinical signs of inflammation.26 These findings
can be related to the diminished existence of large
blood vessels in the buccal gingiva of patients who
smoke compared with those who do not smoke,
along with proliferation of small blood vessels, without significant alterations in vascular density.27 Patients who smoke can show increased periodontal
bone loss even in the absence of dental plaque,28
suggesting that smoking is an important risk factor for
periodontal disease.29,30
Cessation of smoking habits results in stabilization
of the periodontal condition after long-term followup,31,32 although the periodontal conditions of
former smokers have been found to be worse than
those of nonsmokers.33 Our patient was reportedly a
heavy smoker and showed moderate periodontal lesions before orthodontic surgical treatment. However, after surgery, an increase in gingival recession
lesions was observed in maxillary teeth, which could
be associated with the avascular necrosis of the maxilla and diminished blood flow to buccal gingiva, as
the patient reported a return to smoking 3 days after
surgery.
Recent studies34 have suggested that risk factors for
aseptic osteonecrosis can be induced by intravascular
1406
hyperbaric oxygen, and antibiotics should be considered to prevent secondary infection.6,11 Surgical debridement is required to remove necrotic bone fragments, allowing earlier wound healing.6
Hyperbaric oxygen may hasten the delineation of
the necrotic segments and allow a definitive debridement to be done at an earlier time.6,11 However,
hyperbaric oxygenation does not reverse the development of aseptic necrosis once it has started, although it may limit the extent of such necrosis.6 No
protocol for hyperbaric oxygenation has been proposed in literature. In the present case, 20 sessions
were initially planned, but after 15 sessions treatment
was suspended because the patient complained of a
middle earache. Recently, Singh et al13 reported the
treatment of a patient who had experienced avascular
necrosis of the maxilla after an orthognathic surgery
performed 8 years previously. The patient complained
of maxillary pain, pronounced facial asymmetry, malocclusion, and difficulty in eating and was diagnosed
with sinusitis, mobile maxillary teeth, and transverse
alveolar collapse of maxilla, mandibular anterior posterior excess, and facial asymmetry. Treatment was
performed by 30 sessions of hyperbaric oxygenation,
followed by extraction of condemned teeth, debridement of necrotic bone and maxillary right sinus, and
reconstruction of the alveolar ridge with an iliac crest
graft. Three months later, osseointegrated implants
were inserted, and the patient was rehabilitated with
an implant-supported fixed prosthesis with adequate
esthetic outcomes.
Hyperbaric oxygenation is capable of normalizing
the vascular bed within 10 days of treatment, probably because of synthesis of new vascular elements,
and the same size of the vascular bed could be seen
after 30 days. Blood flow, on the other side, was
reduced after 10 days, probably because of new synthesis of blood vessels.12
Heparinization is also reported as a treatment option.6,12 Perfusion to ischemic regions may be improved by reducing blood viscosity, which is a primary factor in blood flow. Heparin administered
subcutaneously reduced morphological tissue damage to the teeth and bone, but this treatment was
complicated by significant hemorrhage from the surgical site.6 However, this treatment was not performed in
the present case, thereby avoiding excessive bleeding
from the wound at the postoperative period.
Careful assessment of the circumstances involved
when small or large bone segments are lost usually
indicates that basic biological principles have been
violated, such as inadequate soft tissue flap design or
impairment of blood supply to maxillary segments.
Excessively long and traumatic surgery, inappropriate
selection of interdental sites for osteotomy, strangulation of the circulation by imprudent use of palatal
PEREIRA ET AL
splints, and excessive stretching of the palatal mucosal pedicle are other causes of compromised wound
healing.9 However, none of these principles was upset during surgery in the present case.
Basic biological principles were strictly followed during and after orthognathic surgery in the present case,
with no ligation of descending palatine vessels to warrant proper bone supply to the osteotomized maxilla,
and no hemorrhage from the surgical site at immediate
postoperative follow-up. These findings suggest that
aseptic necrosis of the maxilla was probably related to
smoking rather than to anatomical irregularities or iatrogeny. This condition was completely resolved with
hyperbaric oxygenation therapy along with antibiotic
therapy and optimal hygiene care of the wound area,
requiring no removal of necrotic bone.
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