Premature exfoliation of primary teeth can be caused by toxicities, metabolic disorders, malignancies, dental causes, and miscellaneous conditions. Specific etiologies include acrodynia from mercury exposure, radiation-induced xerostomia, acatalasia, hypophosphatasia, leukemia-associated gingival enlargement, localized aggressive periodontitis, Papillon-Lefevre syndrome, cherubism, aplastic anemia, and dentin dysplasia. Diagnostic testing may involve blood tests, imaging, biopsies, and microbial cultures to identify the underlying condition leading to premature tooth loss.

1. Etiologies of Premature
Exfoliation of Primary Teeth
Amin Abusallamah

2. Exfoliation of Primary Teeth
Usually begin with the lower anterior
teeth
Usually around the age 6.5 years.

3. Premature Exfoliation of Primary
Teeth can be due to:
Toxicities
Metabolic disorders
Malignancies
Dental causes
Miscellaneous causes

4. Toxicities
Acrodynia
Radiation

5. Acrodynia
“Painful extremities”
Attributed to chronic exposure to mercury
Primarily affects young children. Often
occurs in infants and young children, with
age of onset being between 4 months and
8 years.
Symptoms: irritability, photophobia, pink
discoloration of the hands and feet, and
polyneuritis.
Dental: Inflammation, swelling, and focal
gum erosion can been seen with
subsequent loss of teeth.

6. Radiation
Xerostomia
Increased caries rate
Osteoradionecrosis, leading to
changes in trabeculation, bone loss,
radiolucency.
May lead to increased tooth mobility
and subsequent tooth loss

7. Metabolic
Acatalasia
Chediak-Higashi disease
Gaucher’s disease
Hypophosphatasia (and vit. D
resistant rickets)
Pseudohypophosphatasia
Juvenile diabetes (diabetes mellitus)
Scurvy

8. Acatalasia
AKA Acatalasemia or Takahara's disease. This
syndrome is inherited as an autosomal recessive.
Acatalasia is characterized by absence of the
enzyme catalase.
Poor oral hygiene or mouth injury can lead to
bacterial infection. Certain bacteria produce
hydrogen peroxide. The peroxide destroys
hemoglobin due to lack of catalase thus depriving
the infected area of oxygen and causing necrosis.
Patients may present progressive gangrenous
gingivitis and periodontal disease with
destruction of alveolar bone and loss of teeth.

9. Chediak-Higashi Syndrome
Autosomal recessive trait
Abnormal platelets in these patients result in spontaneous
bleeding and easy bruising.
Eighty five percent of children with CHS develop the accelerated
phase of the syndrome, characterized by a lymphoproliferative
reaction. This leads to unusual lymphoma-like condition generally
leading to death.
The remaining 15% of patients present less severe clinical
manifestations of the syndrome. The accelerated phase can be
triggered by infections with lymphoproliferative viruses or the
Epstein Barr virus.
The oral lesions are a consequence of repeated infections and
they consist of ulcers, markedly hypertrophic gingivitis and severe
periodontal destruction. Periodontal treatment of these patients is
often unsuccessful.
Due to recurrent intraoral infections there is extensive alveolar
bone loss which in most patients leads to tooth exfoliation.

10. Hypophosphatasia
Autosomal recessive
4 groups: perinatal (lethal), infantile,
childhood, and adult
Phenotype can range from premature loss
of decidious teeth to severe bone
abnormality leading to neonatal death.
Characterized by diminished serum levels
of alkaline phosphatase and
phosphoethanolamine in the urine

11. Hypophosphatasia
Abnormal
cementum or lack
of cementum may
lead to
spontaneous
shedding of
primary teeth.
Pulp chambers
may be unusually
large.

12. Hypophosphatasia
Infantile variety
characterized by
severe rickets,
hypercalcemia, and
failure to thrive.
Fatal.
Anterior primary
uniradicular teeth
are shed.

13. Malignancies
Langerhans’ Cell Histiocytosis
Leukemia
Neutropenias
Cyclic Neutropenia
Agranulocytosis

14. Langerhans’ Cell Histiocytosis

15. Langerhans’ Cell Histiocytosis
Acute Disseminated
(Lettere-Siwe) when it
affects infants.
Manifests clinically
hepatosplenomegay
and diffuse radiolucent
bone lesions, “floating
teeth”
This type usually fatal.

16. Leukemia
Oral lesions
characterized by
hyperplastic gingivitis
with cyanotic bluish-
red discoloration.
Diffuse enlargement
of gingiva.
Poor oral hygiene in
can lead to premature
loss of teeth.

17. Dental Causes
Anomalous dental treatment
Caries related infections
Periodontitis
Papillon-Lefevre syndrome
Cherubism

18. Periodontitis
Localized
aggressive
periodontitis (also
known as
prepubertal
periodontitis)

19. Periodontitis
In Localized Juvenile Periodontitis,
there is not much accumulation of
supragingival plaque and/or calculus.
Gingiva is almost normal in
appearance. Minimal subgingival
plaque deposition.

20. Periodontitis
Radiographs show
marked destruction
of alveolar bone
with vertical pocket
formation.
Advanced cases
present tooth
mobility and
malposition which
may lead to teeth
loss.

21. Papillon-Lefevre syndrome
Key features are
palmar and plantar
hyperkeratosis.
Dentally:
attachment and
bone loss result in
premature loss of
primary and
permanent teeth.

22. Papillon-Lefevre syndrome

23. Miscellaneous Causes
Dentin Dysplasia
Tumors of the jaw
Aplastic anemia
Scleroderma
Facial hemihypertrophy
Cherubism (familial fibrous dysplasia)
Systemic infections, i.e. tuberculosis
Odontodysplasia

24. Dentin Dysplasia
Autosomal dominant
Two types. Type 1 known as radicular
dentis dysplasia, and affects both
dentitions. Characteristics are markedly
short and pyramidal roots.
Type 1 is associated with premature loos
of teeth.
Teeth lost generally due to trauma since
the short roots lead to easy avulsion.

25. Dentin Dysplasia
Note the characteristically short and
pyramidal roots.

26. Aplastic Anemia
Anemia is a common blood disorder,
which is caused when there is a drop
in hemoglobin or hematocrit in the
blood.

27. Aplastic Anemia
Sore or swollen
tongue (glossitis)
Oral thrush
Bleeding gingiva
Impaired wound
and tissue healing

28. Cherubism

29. Cherubism
Autosomal dominant fibro-osseous
lesion of the jaws involving more
than one quadrant that stabilizes
after the growth period, usually
leaving some facial deformity and
malocclusion.

30. Cherubism

31. Cherubism
“Ground glass" appearance
Unilocular or multilocular
bilateral expansive
radiolucenices
Randomly distributed teeth
and multiple unerupted
teeth
Faint radiopacities
resembling residual bones
sometime present at
puberty
Radiographic appearance
becomes more
radiopaque after stabilization
period

32. Odontoplasia
Also known as “ghost teeth”
Affected teeth are poorly mineralized and
radiographically appear evanescent
They generally fail to erupt but if they do they
have the consistency of gelatin. Often need to be
extracted.

33. Misc. Causes (con’t.)
Natal and neonatal teeth
Trauma
Extreme bruxism
Finger habit

34. Diagnostic Test for premature
exfolioation of primary teeth
CBC–Hematrocrit, hemoglobin,
platelets, RBC, WBC
Differential leukocyte count
Cell morphology
Serum levels- Phosphate, calcium,
alkaline phosphatase, blood glucose
Erythrocyte sedimentation rate

35. (con’t.)
Urinalysis- glucose,
phosphoethenolamine
Skull survey
Culture for anaerobic bacteria
Gingival biopsy
Tooth biopsy
Neutrophil chemotaxis
CD11b/CD18 assays

36. References
http://www.dent.ohio-
state.edu/postdocgd/Oncology/OralOncology06RadiationCompha
ndout
df
www.dent.ucla.edu/ftp/pic/visitors/teethloss
http://www.dental.mu.edu/oralpath/lesions/cherubism/cherubism
.htm
E.medicine.com
Jordan, RC. Diagnosis of periodontal manifestations of
systemic
Volume 34 Periodontology 2000
diseases. Issue 1 Page 217 - February 2004.
Pictures from Dr. Casamassimo’s collection
Dr. Eileen Cunnane, Eastman Dental Center, Rochester, NY