Oral Manifestations of Endocrinal Disorders
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Transcript of Oral Manifestations of Endocrinal Disorders
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Oral Manifestation of Pituitary Disorders
Patients with GH excess have a characteristic coarse
facial appearance because of the thick rubbery skin,
enlarged nose, and thick lips.
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They have macrognathia, disproportionate mandibular
growth manifesting as mandibular prognathism, and
generalized diastemata .
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They also have anterior open bite and malocclusion
because of the macrognathia and tooth migration.
Intraorally, excessive soft tissue growth usually
presents as macroglossia and hypertrophy of the
pharyngeal and laryngeal tissues, making the
patient susceptible to sleep apnea.
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Dental radiographs may demonstrate large pulp chambers
(taurodontism) and excessive deposition of cementum on the
roots (hypercementosis).
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Individuals with GH deficiency present with disproportionate
delayed growth of the skull and facial skeleton, giving them a
small facial appearance for their age.
Tooth formation and growth of the alveolar regions of the
jaws are abnormal and may be disproportionately smaller
than adjacent anatomic structures, leading to tooth crowding
and malocclusion.
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Eruption of primary and secondary dentition and
shedding of deciduous teeth are delayed.
Due to the dental anomalies and crowding, there is ahigh tendency for plaque accumulation, and
patients have difficulty maintaining good oral
hygiene. Therefore, these patients may be prone to
gingivitis and periodontal disease.
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Hyperadrenocorticism (Glucocorticoid Excess or Cushings Syndrome )
The primary orofacial feature of Cushings syndrome is a
round, moon face due to muscle wasting and accumulation
of fat.
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Surface capillaries in the face and other skin regions
become fragile, rendering them readily susceptible
to hematomas after mild trauma.
Long-standing Cushings syndrome produces
delayed growth and development, including skeletal
and dental structures.
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Many of the systemic findings of Cushings syndrome are
similar to those seen in patients on moderate- to high-dose
glucocorticoid therapy, and these patients are considered to beimmunosuppressed. Therefore, oral signs and symptoms of
immunosuppression can be seen, including oral candidiasis,
recurrent herpes labialis and herpes zoster infections, gingivaland periodontal diseases, and impaired wound healing.
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Hypoadrenocorticism(Glucocorticoid Deficiency or Addisons Disease)
The primary orofacial feature ofAddisonsdisease is unusual
skin pigmentation, most intensely over sun exposed areas.
The mucocutaneous junctions undergo increased
pigmentation, including the lips, but it can also occur on
intraoral mucosal surfaces such as the gingival margins,
buccal mucosa, palate, and lingual surface of the tongue
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The oral pigmentations appear as irregular spots that range
from pale brown to gray or black.
The treatment ofAddisonsdisease includes administration of
corticosteroids. This increases the risk of immunosuppression
with concomitant susceptibility to oral candidiasis, recurrentherpes labialis and herpes zoster infections, gingival and
periodontal diseases, and impaired wound healing.
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Hyperthyroidism-Hyperthyroidism can exacerbate the patients response to
dental pain and anxiety.
-Routine examination of the head and neck may disclose signs ofthyroid disease, including protrusion of the eyes, excesssweating, enlargement of the thyroid and difficulty inswallowing.
-Patients may have increased susceptibility to dental cariesand periodontal diseases.
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Hypothyroidism-In hypothyroidism, orofacial findings include facial
myxedema, enlarged tongue (macroglossia) and and a
hoarse voice.
- Compromised periodontal health, delayed tooth eruption,
delayed wound healing, Salivary gland enlargement, changes
in taste, and burning mouth symptoms have also been
reported.
Hashimotos thyroiditis has been associated with xerostomia
and impaired salivary output.
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Hypersecretion of female sex hormones commonly occurs in pregnancy:
Such as bilateral brown facial pigmentation (melasma),
which disappears after delivery of the newborn baby.
High levels of female sex hormones cause increased capillary
permeability, making them susceptible to gingivitis
(pregnancy gingivitis), gingival hyperplasia, and pyogenic
granuloma (pregnancy tumor). These factors may complicate preexisting periodontal
disease.
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Oral Manifestations of
Parathyroid Gland Disorders
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Hyperparathyroidism The primary clinical orofacial signs and symptoms of
hyperparathyroidism are reflections of the systemic effects
of hypercalcemia. Long-standing hypercalcemia causes
generalized osteoporosis, which is visible on dental
radiographs. Patients develop cortical resorption and
rarefactions, loss of trabeculation presenting as ground-
glassappearance.
Partial or total loss of lamina dura, lytic lesions, and
metastatic calcifications.
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Thinning and eventual loss of the cortical bone of the maxilla
and mandible may occur, especially on the lower border of
the mandible. Severe cases result in spontaneous mandibular
fracture
The lytic jaw lesions or brown tumors can increase in size,
causing the bony cortex to expand, ultimately becomingdestroyed. These tumors rarely expand into the periosteum
but can produce gingival swelling.
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Fully developed teeth are not affected except that they
appear more radiopaque.
Due to bony changes, the teeth become mobile, drift,
and cause malocclusion.
Increased periodontal pocketing, root resorption, and
dental pain.
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Hypoparathyroidism
In hypoparathyroidism, hypocalcemia produces increased
muscular and peripheral nerve irritability .Painful muscular
spasms affect oral and laryngeal muscles.
Despite low serum calcium levels, the maxilla and mandible
are abnormally dense, with well-calcified trabeculae.
If the hypoparathyroidism is part of an autoimmunepolyendocrinopathy syndrome, oral mucocutaneous
candidiasis may be present in an acute or chronic form.
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If hypoparathyroidism occurs when teeth are stilldeveloping, there will be abnormalities in the appearanceand eruption pattern. There may be enamel hypoplasia, andpoorly mineralized dentin.
Other dental findings include malformed teeth, anodontia,short blunt root apices, elongated pulp chambers (someoccluded by pulp stones, even in the primary dentition),impacted teeth, and mandibular exostoses.
If hypoparathyroidism occurs after dental development,there are no abnormalities seen in erupted teeth.
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