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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.

They

have macrognathia, disproportionate mandibular

growth manifesting as mandibular prognathism, and generalized diastemata .

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.

Dental radiographs may demonstrate large pulp chambers

(taurodontism) and excessive deposition of cementum on the roots (hypercementosis).

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.

Eruption of primary and secondary dentition and

shedding of deciduous teeth are delayed.


Due to the dental anomalies and crowding, there is a

high tendency for plaque accumulation, and patients have difficulty maintaining good oral hygiene. Therefore, these patients may be prone to gingivitis and periodontal disease.

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.

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.

Many of the systemic ndings of Cushings syndrome are

similar to those seen in patients on moderate- to high-dose glucocorticoid therapy, and these patients are considered to be immunosuppressed. Therefore, oral signs and symptoms of

immunosuppression can be seen, including oral candidiasis,


recurrent herpes labialis and herpes zoster infections, gingival and periodontal diseases, and impaired wound healing.

Hypoadrenocorticism (Glucocorticoid Deficiency or Addisons Disease)


The primary orofacial feature of Addisons disease 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

The oral pigmentations appear as irregular spots that range

from pale brown to gray or black.


The treatment of Addisons disease includes administration of

corticosteroids. This increases the risk of immunosuppression with concomitant susceptibility to oral candidiasis, recurrent herpes labialis and herpes zoster infections, gingival and periodontal diseases, and impaired wound healing.

Hyperthyroidism
-Hyperthyroidism can exacerbate the patients response to dental pain and anxiety. -Routine examination of the head and neck may disclose signs of thyroid disease, including protrusion of the eyes, excess sweating, enlargement of the thyroid and difficulty in swallowing. -Patients may have increased susceptibility to dental caries and periodontal diseases.

Hypothyroidism
-In hypothyroidism, orofacial findings include facial

myxedema, enlarged tongue (macroglossia)


hoarse voice.

and and a

- 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.

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.

A decrease in gonadal hormones at menopause is

associated with Decrease in salivary flow .These may predispose individuals to dental caries, dysgeusia, unpleasant metallic taste, oral candidiasis and increased risks of gingivitis and periodontitis. After dental extractions, unrestored edentulous ridges rapidly undergo resorption. Postmenopausal women have increased susceptibility to osteoporosis, so dental radiographs may demonstrate hypocalcified bone.

Oral Manifestations of Parathyroid Gland Disorders

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 groundglass appearance.
Partial or total loss of lamina dura, lytic lesions, and

metastatic calcifications.

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 becoming


destroyed. These tumors rarely expand into the periosteum but can produce gingival swelling.

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.

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 autoimmune

polyendocrinopathy

syndrome,

oral

mucocutaneous

candidiasis may be present in an acute or chronic form.

If

hypoparathyroidism occurs when teeth are still developing, there will be abnormalities in the appearance and eruption pattern. There may be enamel hypoplasia, and poorly mineralized dentin. Other dental findings include malformed teeth, anodontia, short blunt root apices, elongated pulp chambers (some occluded 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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