Necrotizing Sialometaplasia in a Patient With an Eating Disorder

Necrotizing Sialometaplasia in a Patient
With an Eating Disorder: Palatal Ulcer
Accompanied by Dental Erosion Due
to Binge-Purging
Tomoaki Imai, DDS, PhD,* and Masahiro Michizawa, DDS, PhDy
This report describes a case of necrotizing sialometaplasia (NS) accompanied by significant dental erosion
of the maxillary teeth of the palatal surfaces owing to chronic self-induced vomiting. This observation contributed to the determination of an immediate and appropriate provisional diagnosis of NS in a patient with
an eating disorder, which subsequently was confirmed histopathologically as NS. The diagnostic challenges presented by NS associated with eating disorders and its management are discussed.
Ó 2013 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 71:879-885, 2013
However, Kaplan et al7 recently reported an apparently higher incidence in female patients. This lesion
can be misdiagnosed histologically as a malignancy
owing to the difficulty in the differential diagnosis
from squamous cell carcinoma or mucoepidermoid
carcinoma.6 Unlike squamous cell carcinoma, the
lobular architecture and bland morphology of metaplastic squamous cells are preserved in NS without significant cellular atypia. NS also can be differentiated
from mucoepidermoid carcinoma by the presence of
incorporated luminal elements of remnant mucous
cells and mucin pools into metaplastic islands,
whereas mucoepidermoid carcinoma often exhibits
features of cystic spaces lined by neoplastic cells.8
Although the etiology has not been established, it
is generally accepted to involve ischemic circulation of
the salivary gland lobules followed by an inflammatory
response. Clinical examination shows that ischemia typically develops in the oral cavity as a consequence of
smoking, local injury, blunt force trauma, denture wear,
or surgical procedures.4,6 In other sites, NS can occur
in the trachea after intubation and the larynx owing
to atheromatous embolization.9,10 It also has been
reported in patients with other conditions, including
pregnancy, diabetes, sickle cell disease, Buerger disease, lymphoma, upper respiratory tract infections,
cocaine abuse, bulimia, and chronic vomiting.4,11-14
Patients with EDs carry a negative mental image of
their own body and a lack of self-esteem and, accordingly, are often defensive and unwilling to fully disclose
their conditions when visiting a dental clinic with any
oral symptom.1,2,15 A diagnosis of NS in these patients
is thus largely dependent on the identification of an
Eating disorders (EDs) are a group of psychopathologic conditions that affect the relation between
a patient’s body and food consumption, leading to
abnormal eating behavior and potential or overt medical complications.1,2 Mucosal, dental, and salivary
manifestations have been reported in patients with
EDs, and the management of their oral health
remains challenging.1 In addition to these oral
pathologies, necrotizing sialometaplasia (NS) is considered an uncommon but emerging associated
complication.1,3
NS is a self-limiting inflammatory condition that
commonly occurs as a deep ulcer in the posterior
hard palate.4 This lesion also can be found in major salivary glands and at other sites that contain salivary
glands, including the nasal cavity, trachea, buccal
mucosa, maxillary sinus, tonsil, and tongue.3-5 The
incidence appears higher in male patients, with
a male-to-female ratio of approximately 2:1, and particularly is increased in men older than 40 years.4,6
Received from the Department of Oral and Maxillofacial Surgery,
Saiseikai Senri Hospital, Suita, Osaka, Japan.
*Division Chief.
yFormer Chief.
Address correspondence and reprint requests to Dr Imai:
Department of Oral and Maxillofacial Surgery, Saiseikai Senri
Hospital, 1-1-6 Tsukumodai, Suita, Osaka 565-0862, Japan; e-mail:
[email protected]
Ó 2013 American Association of Oral and Maxillofacial Surgeons
0278-2391/12/01627-8$36.00/0
http://dx.doi.org/10.1016/j.joms.2012.10.033
879
880
NECROTIZING SIALOMETAPLASIA IN EATING DISORDERS
objective diagnostic cue. This report describes a case
of NS accompanied by significant dental erosion of
the maxillary teeth of the palatal surfaces owing to
chronic self-induced vomiting. This observation contributed to the determination of an immediate and
appropriate provisional diagnosis of NS in a patient
with an ED, which subsequently was confirmed
histopathologically as NS. The diagnostic challenges
presented by NS associated with EDs and its management are discussed.
induration and did not penetrate the nasal cavity. Regional cervical lymphadenopathy was not detectable
by palpation. The right side of the submandibular
gland was slightly enlarged and tender, whereas the
parotid and lacrimal glands were not swollen. Hyposalivation was observed, but keratoconjunctivitis sicca
and arthralgia were not apparent. There was dental
erosion involving the dentin on the palatal surfaces
of the maxillary anterior and posterior teeth and the
enamel on the occlusal surfaces of the maxillary molars. This erosive pattern indicated an association
with intrinsic acid regurgitation or vomiting, likely
an ED. The occlusal surfaces of the dentition displayed
no facets created by attrition, which produces a similar
amount of wear on the opposing teeth. Dental caries
and periodontal disease were not apparent. Laboratory tests showed hypokalemia (potassium level,
2.7 mEq/L) and iron deficiency hypochromic anemia
(hemoglobin, 11.5 g/dL; mean corpuscular volume,
74.4 fL; mean corpuscular hemoglobin, 22.7 pg; serum
iron level, 24 mg/dL; unsaturated iron-binding capacity,
343 mg/dL). Hematologic tests did not show an inflammatory response. Hepatic and renal functions and
serum levels of amylase and soluble interleukin-2 receptor were within normal limits. Serologic testing
ruled out intraoral syphilis. Based on these findings,
the authors provisionally diagnosed NS in the patient
with an ED with binge-purging symptoms, without
inquiring about the patient’s dietary habits to avoid
losing her trust. The patient refused to consent to imaging procedures, including computed tomography
and magnetic resonance imaging, but did approve
Report of Case
A 26-year-old woman complaining of an ulcerative
stomatitis on the posterior hard palate was referred
to the authors’ center. The patient reported that a painful lesion had developed in this location 12 days previously, which was followed by submucosal fluctuation
and rupture of the ulcer 4 days later. The patient’s
height and weight were 160 cm and 40 kg, respectively (body mass index, 15.6 kg/m2). She was afebrile
and had not experienced fatigue or nocturnal sweating. She was a nonsmoker with no apparent history
of alcohol abuse, recent surgery, or trauma. Although
she described the use of psychiatric services on the interview sheet, she refused to provide further details.
She was not prescribed antipsychotic or antianxiety
drugs at that time.
Intraoral examination disclosed a 12- 13-mm ulcer
12 mm deep, with the necrotic surface located on the
right side of the hard palate (Fig 1). The ulcer had
thickened keratotic borders without tenderness or
FIGURE 1. Mirror views of the ulcer in the hard palate and dental erosion. A, The base of the lesion is covered with necrotic debris at the initial
visit. The occlusal surfaces of the posterior teeth have depressed cusps and edges, raising the level between the metal inlays and the adjacent
tooth surface (arrowheads). Palatal surfaces show a polished cervical appearance of the wear facets involving dentin. In anterior untreated
teeth, loss of palatal contour and exposure of dentin are apparent (arrows). B, The ulcer is almost completely healed after 3 weeks.
Imai and Michizawa. Necrotizing Sialometaplasia in Eating Disorders. J Oral Maxillofac Surg 2013.
881
IMAI AND MICHIZAWA
a histopathologic examination to confirm the inflammatory condition and to exclude neoplasms such as
carcinoma or lymphoma.
During the patient’s initial visit, the authors performed an incisional biopsy of the anterior aspect of
the ulcer, including the peripheral margin (Fig 2).
The specimen featured a mucosal fragment lined
with hyperplastic parakeratinized epithelium. Although the underlying lobular architecture of the palatal salivary gland tissue was maintained, some lobules
were necrotic with stromal inflammatory infiltration
secondary to extravasation of mucin. Squamous metaplasia of ducts was evident with a benign nuclear morphology. These findings were compatible with NS.
On her next visit, conducted in a comfortable setting, the patient was presented with the histopathologic diagnosis and the indication of a possible
background of ED with binging-purging. The patient
was relieved to learn that her lesion was not malignant
and then admitted to binge eating, self-induced vomiting, occasional laxative use, and amenorrhea. The EDs
had persisted as anorexia nervosa for more than
10 years and binging-purging developed in the past
several years. These inappropriate events had become
temporarily more frequent before the manifestation of
the initial symptom of the lesion on her palate. Scarring over the dorsum of the patient’s hands (Russell
sign) was not evident. During the stable period, vomiting could almost always be self-induced without the
application of pressure with a finger. Upon worsening
of binging-purging, she admitted to an increase in undue mechanical stress to the palate with food or instruments. The rapid development of the palatal ulcer
caused the patient concern, which likely led to a stable
level of abnormal eating behaviors by the time of her
initial visit. The patient continued regular visits to
her psychiatric doctor for further care. Although professional dental examinations had been discontinued
for several years, the patient agreed to resume regular
visits to her dentist. The palatal ulcer healed spontaneously within 4 weeks without complications.
Discussion
DIFFERENTIAL DIAGNOSIS OF PALATAL ULCER
The clinical differential diagnosis of a palatal ulcer
generally includes traumatic, inflammatory, and infectious processes and malignant neoplasms and requires clinical information, including the course
(acute or chronic), symptoms (painful or not), and
a patient’s background. Self-inflicted injury by patients with EDs and depression based on a dislike
of the body might contribute to the diagnosis.16
The relatively rapid appearance of an ulcer and the
lack of induration at its borders are likely to indicate
an inflammatory condition rather than invasive carcinoma or salivary gland tumors, although nonHodgkin lymphoma, in particular extranodal natural
killer/T-cell lymphoma, and the possibility of other
sarcomas cannot be completely excluded. A necrotic
deep ulcer emerging after possible causative mechanical stress and followed by mucous swelling that can
be fluctuant is clinically consistent with NS. With regard to specific inflammatory diseases, serologic testing ruled out intraoral syphilis. An intraoral ulcer
owing to tuberculosis is painful,17 but the patient
did not report spontaneous pain or severe tenderness
in the ulcer at her initial visit or exhibit the
FIGURE 2. Microscopic appearance of a specimen from the incisional biopsy (hematoxylin and eosin stain). A, Necrotic mucous glands and
squamous metaplastic islands show scattered stromal inflammatory infiltration (magnification, 100). B, Metaplastic cells show a benign
nuclear morphology with minimal pleomorphism and no atypical mitotic figures (magnification, 400).
Imai and Michizawa. Necrotizing Sialometaplasia in Eating Disorders. J Oral Maxillofac Surg 2013.
882
NECROTIZING SIALOMETAPLASIA IN EATING DISORDERS
characteristic general symptoms of tuberculosis, including fatigue, slight fever, and cough. Intraoral invasive fungal infections such as aspergillosis, a rare
condition, usually present as a necrotic ulcer in an
immunocompromised host, such as chemotherapyinduced granulocytopenia or acquired immunodeficiency syndrome.18 Wegener granulomatosis, an autoimmune disease characterized by systemic
vasculitis of small arteries and veins, typically presents in the head and neck as rhinitis and sinusitis, accompanied by cough and hemoptysis. The oral
mucosa can be involved as granular erythematous
gingiva and uncommonly as a palatal ulcer.19
An accurate diagnosis is occasionally made only
after several alternative tracks of thinking, and that
of NS in patients with EDs is no exception. Previous
cases have been misdiagnosed histopathologically as
carcinoma at initial biopsy and surgically resected.3,20
In others, no ED-associated intraoral symptoms other
than palatal NS were assessed or presented.7,21,22
The present case is unique in that dental erosion
as an objective intraoral clue potentially shared an
associated background with the ulcer and thus
aided in providing an immediate and appropriate
provisional diagnosis of NS, which was subsequently
confirmed by histopathology (Table 1).
An incisional biopsy with an equivocal clinical diagnosis such as palatal ulcer might lead to a misdiagnosis
without consideration of the differential diagnosis of
NS based on histopathology. It is important to note
that an accurate clinical diagnosis helps guide the pathologist. Further, the possibility that a malignancy is
simultaneously accompanied by NS should be investigated by biopsy.23
also can be associated with vomiting-associated oral
manifestations, such as dental erosion.25
In the present patient, whose body weight was
approximately 75% of that expected for her age, it
was concluded, based on her psychiatric consultation,
that her condition was best described as anorexia of
the binge-eating/purging type. In contrast, to the
authors’ knowledge, all previous cases of NS associated with EDs reported in the literature have been
categorized as bulimia,3,7,20-22 although body weight
and blood test results were not reported. The
patients studied in these and the present report
share binging-purging symptoms. Anorexia with these
symptoms features highly diagnostic transitions with
bulimia during the clinical course.26 As advocated by
Frydrych et al,27 it would be reasonable to assume
that the distinction in EDs between vomiting and
nonvomiting subtypes is important with respect to
the effects of habitual behavior on intraoral tissues.
EATING DISORDERS WITH BINGING-PURGING
SYMPTOMS
Anorexia nervosa and bulimia nervosa are the most
commonly encountered EDs. Bulimia is characterized
by recurrent episodes of binge eating, followed by
compensatory behaviors, including self-induced vomiting, excessive exercise, and misuse of laxatives, enemas, and other medications.1 Individuals with
bulimia are frequently of normal body weight or
even slightly overweight.24 In contrast, patients with
anorexia maintain a distorted body image, with a fear
of gaining weight, and therefore maintain body
weights less than 85% adjusted for age. Further, anorexics are more likely to develop microcytic anemia
with iron deficiency, whereas bulimics usually are
not anemic.24 Anorexia is further categorized into restricting or binge/purge subtypes. Individuals with
the latter subtype regularly engage in binge eating
and inappropriate compensatory behaviors to maintain a low body weight.24 Like bulimia, this subtype
ORAL MANIFESTATIONS IN EATING DISORDERS
Potential complications of EDs in the oral and maxillofacial regions include dental erosion, caries, decreased salivary flow, periodontal diseases, atrophic
mucosa, and sialosis.1 During vomiting, the gastric
contents initially confront the palatal surface of the
maxillary dental arch. This surface also often contacts
the tongue surface, which retains gastric fluid among
its filiform papillae, resulting in the erosion of polished
surfaces. Further, the palatal surface of the maxillary
dental arch is unlikely to receive direct salivary protection because of its relatively long separation from the
openings of the major salivary glands. Frequent vomiting thus leads to the predominantly lingual erosion of
the maxillary anterior and posterior teeth.1 Eroded
enamel exhibits uniform, spoon-like surfaces, rounded
margins, loss of contour of untreated teeth, and
notched incisal surfaces of the anterior teeth.1 Moreover, mechanical wear leads to abrasion characterized
by a sharply cut, flat, and angled appearance.1 Extrinsic acid usually causes dental wear on the facial and occlusal surfaces as a result of its intraoral entrance from
the anterior aspect.
Sialosis is characterized by noninfectious swelling of
major salivary glands, particularly the bilateral parotids
glands. This manifestation frequently can be found in
patients who vomit or purge.2 In the present case, sialosis might have developed as unilateral swelling of the
submandibular gland, although cases without parotid
enlargement are an unusual pattern of sialosis.
Compensatory behaviors associated with EDs, such
as frequent self-induced vomiting or misuse of laxatives, can alter the electrolyte balance and decrease
saliva flow owing to dehydration.2 Although no serologic assays are available to confirm this diagnosis,
IMAI AND MICHIZAWA
Table 1. SUMMARY OF NECROTIZING SIALOMETAPLASIA IN PATIENTS WITH EATING DISORDERS WITH BINGING-PURGING SYMPTOMS
Case
Schoning et al21
(1998)
Age/
Tooth
Gender Erosion
Blood Tests
Provisional
Diagnosis
Biopsy
Histopathologic
Diagnosis
Treatment
Enlarged Major
Salivary Glands
History
of EDs
20/F
NR
NR
NR
incisional
NS
observation
NR
3 yr
21/F
Scully and Eveson22 29/F
(2004)
Solomon et al20
32/F
(2007)
NR
NR
NR
bulimia not implicated
NR
NS
incisional
incisional
NS
NS
observation
observation
yes
NR
NR
NR
bilateral parotid
glands
none
Carlson3 (2009)
32/F
NR
NR
NR
Kaplan et al7
(2012)
Present case
33/F
NR
NR
NR
excisional 1st, MEC; 2nd, SCC additional resection
owing to histopathologic
misdiagnosis
incisional 1st, MEC; 2nd, SCC surgical resection owing to NR
histopathologic
misdiagnosis
incisional NS
observation
NR
3 yr
uncertain
duration
uncertain
duration
26/F
yes
NS
hypokalemia and
iron deficiency
hypochromic anemia
incisional
NS
observation
unilateral
submandibular
gland
uncertain
duration
uncertain
duration
>10 yr
Abbreviations: EDs, eating disorders; F, female; MEC, mucoepidermoid carcinoma; NR, not reported; NS, necrotizing sialometaplasia; SCC, squamous cell carcinoma.
Imai and Michizawa. Necrotizing Sialometaplasia in Eating Disorders. J Oral Maxillofac Surg 2013.
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NECROTIZING SIALOMETAPLASIA IN EATING DISORDERS
hypokalemia may be a specific predictor of recent
vomiting episodes.28 The degree of dental erosion
may be related to the duration of binging-purging.29
In the present case, findings of dental erosion accompanied by serum hypokalemia were consistent with
the clinical history of a relatively long history of an
ED with binging-purging and an increased frequency
of these episodes before the manifestation of NS.
Among the possible predisposing systemic conditions for NS, diabetes with atherosclerosis,14 autoimmune diseases with related vasculitis,5 and Buerger
disease with Raynaud phenomenon13 can cause a narrowing of peripheral vessels, leading to a compromised
blood supply.11 Intriguingly, peripheral vasculopathy
also has been reported in patients with EDs.30,31
Sickle cell anemia predisposes to ischemia owing to
an increase in nonfunctional erythrocytes and blood
viscosity and has been hypothesized to be a potential
underlying cause of NS.11
Local injury with ischemia is considered an etiologic
component of NS.4,5,32 Rye et al13 reported that ischemia likely has a greater impact in the posterior hard
palate, which is supplied primarily by a branch of
the greater palatine artery, whereas surrounding areas
are supplied from multiple vessels. In patients who
vomit/purge, undue pressure or microtrauma to the
posterior palatal mucosa owing to rapid food ingestion
or use of a finger or instrument to induce vomiting is
considered a local predisposing factor for NS.21,22
When insufficiently protected by a decreased saliva
output, the mucosa is likely to be fragile because of
direct long-term gastric acid-induced chemical injury
and potential nutritional deficiencies.1 Because the
pain threshold is increased in patients with EDs, especially those with binging-purging,33 this characteristic
also might contribute to the development of NS
in EDs.
In the present case, temporary worsening of
binging-purging before the development of NS would
likely have led to an increase in traumatic stress and
chemical exposure of the palate. Iron deficiency hypochromic anemia could compromise the steady supply
of oxygen to the palate locally affected by frequent abnormal eating behaviors. These systemic and local factors might trigger irreversible ischemic changes in the
palatal salivary gland tissues for a short time. Details of
the mechanisms of NS against a background of EDs
with binging-purging await the accumulation of additional experimental and clinical studies.
Burkhart et al15 presented a detailed and systematic
protocol for approaching patients with suspected
bulimia, which aimed to encourage them to agree to
comprehensive oral health treatment. Using a secure
and private location at an appropriate time and with
particular awareness of a patient’s body language,
the clinician should suggest possible causes of the
oral symptoms, establish the patient’s associations
with foods, and assess the patient’s body-image concepts and eating habits. The approach in the present
case was consistent with these methods. A systematic
approach to establishing a diagnosis of NS associated
with EDs should aid clinicians in convincing the patient to consider resuming preventive dental care
aimed at minimizing damage to the enamel and oral
soft tissues.
The development of oral manifestations in EDs
might potentially exacerbate its etiologic factors,
such as a lack of self-esteem or a dislike of one’s
body.1 Considering the gap between the dramatic progression and striking appearance of the ulcer and its
self-limiting nature, the proper diagnosis and appropriate management of NS based on an appropriate evaluation of hard and soft oral tissues are challenging
responsibilities for oral specialists. A deep palatal ulcer
that occurs subsequent to a painful erythematous
swelling in a young adult woman with a suspected
ED with binging-purging should make NS a differential
diagnostic priority.
Acknowledgments
The authors thank Dr Fumiyoshi Kojima, Department of Pathology, Saiseikai Senri Hospital for the histopathologic diagnosis, and
Dr Masahiro Iwakiri, a psychiatrist, for consultation.
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