EATING DISORDERS

I. DEFINITION
The eating disorders are syndromes that are classified on the basis of the
clusters of symptoms with which they present. They are not specific diseases with a
single common cause, course, or pathophysiology. This paper will focus on well
defined eating disorders of anorexia nervosa and bulimia nervosa.
A. CRITERIA FOR ANOREXIA NERVOSA
According to the latest Diagnostic and Statistical Manual of Mental Disorders
Fourth Edition (DSM-IV) criteria:

Refusal to maintain body at or above a minimally normal weight for

age and height. In the absence of other physical illness, anyone
maintaining a weight less than 85%of that expected should be
thoroughly interviewed for other symptoms of anorexia nervosa.
Intense fear of gaining weight. Anorexic patients fear of gaining weight
exists even when they are emaciated. They will develop rigorous
exercise programs and severely restrict their total food intake in order
to prevent weight gain.
The central concern of weight and shape in the evaluation of the self,
in addition to a reference to the denial of the serious consequence of
weight loss.
Amenorrhea.

SUBTYPES:

The restrictor type

The binge purger type

B. CRITERIA FOR BULIMIA NERVOSA

Bulimia is characterized by uncontrollable binge-eating episodes, often
followed by purging behaviors such as vomiting or the use of laxatives.
Diagnostic criteria for Bulimia Nervosa:

Recurrent episodes of binge eating . An episode of binge eating is

characterized by both of the following:
- In a discrete period of time (e,g, within any 2-hour period),
eating an amount of food that is larger than what most people would
eat during a similar period of
time and under similar circumstances.
- A sense of lack of control over eating during the episode.

Recurrent inappropriate compensatory behavior to prevent weight gain

, such as self induced vomiting; misuse of laxatives, diuretics, enemas
or other medications; fasting or exercising excessively..
The binge eating and inappropriate compensatory behaviors both
occur, on average, at least twice a week for 3 months.
Self evaluation is unduly influenced by body shape and weight.
The disturbance does not occur exclusively during episodes of anorexia
nervosa.

SUBTYPES:

Purging
Non purging

C. ORAL MANIFESTATIONS
Early identification of oral changes by the dental practitioner and referral to
medical and psychiatric therapists can reduce the risk of further physical damage in
the body or greater loss of tooth surface enamel.

Severe erosion of the enamel on the lingual surfaces of the maxillary teeth cardinal oral
manifestation of eating disorders, due to
acids from chronic vomiting.

Parotid enlargement - as a result of starvation

Mandibular teeth may be affected.

Dental caries
- due to an excessive carbohydrate intake, poor oral
hygiene and changes that
occur in the saliva.
- Bulimics during binge periods consume huge amounts of sugar,
followed by
sugar drinks to relieve thirst after vomiting.
- Anorexics whose diet is limited but if under care of a physician
are also
susceptible to
dental caries because some
medications such as dextrose
tablet, dietary supplements and
vitamin C drinks contain sugar.
- Neglect of oral hygiene can be seen in both bulimic and
anorexic patients due
mainly to upset in daily routine.
- Anorexic patients have been found to have decreased salivary
pH and
decreased buffering action, with low pH
contributing to caries.
Palatal ulcerations - caused by use of finger or foreign object to induced gag
reflex and
regurgitation.

D. Management

Refer to other practitioners.

Support of the patient physically, by treatment of tooth desensitization and

esthetics.
Support of the patient psychologically, by demonstrating a caring and
compassionate attitude.

PLASMA CELL NEOPLASIA

I. DEFINITION
Is a group of related malignant disorders of terminally differentiated B
lymphocytes (plasma cells), of which plasma cell myeloma or multiple myeloma is
the most common (90% of cases).

This condition is characterized by bone marrow multifocal infiltration by

malignant plasma cells. There are typically multiple destructive lesions or diffuse
demineralization of bone. The tumour cells secrete a homogenous, complete or
partial, immunoglobulin molecule, an M component or para protein, most commonly
IgG or IgA.
II. ETIOLOGY

Genetic predisposition - is suggested by an increase incidence of multiple

myeloma in first degree relatives of patients with plasma cell neoplasia and
the higher frequency of multiple myeloma in blacks.
Ionizing radiation - has been incriminated in the etiology as evidence by the
long term survivors of Hiroshima and Nagasaki increased incidence of
multiple myeloma.
Chronic antigenic stimulation - some cases of multiple myeloma have been
associated with chronic infections such as HIV and chronic osteomyelitis and
with chronic inflammatory disorders (rheumatoid arthritis). A two hit
hypothesis is proposed by which (1) antigenic stimulation leads to reactive,

polyclonal proliferation of B- lymphocytes and (2) a subsequent mutagenic

event establishes a single malignant clone.
III. ORAL MANIFESTATION

Maxillary or mandibular lesions - in a radiograph this lesions will appear as

multiple punched out
areas of radiolucency.
- premolar- molar area and the coronoid process are
the
favored sites.
- common symptoms: swelling, numbness, pain,
loosening of
the teethand formation of soft tissue
plasmacytomas.

Root resorption and loss of lamina dura may be found.

Amyloid like deposition in the gingiva and tongue.

IV. DENTAL MANAGEMENT

Patients are prone to postoperative hemorrhage due to thrombocytopenia.

Development of dental amyloidosis.
Dental hygiene care should focus on controlling infections associated with a
compromised immune system.
Patients being treated with bisphophonates must be monitored closely for the
development of osteonecrosis of the jaw.
Educate patient about the necessity of reporting unusual sores or painful
areas in the mouth.