EVALUATION OF PARATHYROID

HORMONE AND ITS EFFECTS ON

ORAL

By Ez Al-Deen M.Abdul-Hassan Nisreen Adel Jawad

Ali Saleem Radhi Awfa Khudair Abbas
Zahraa Saleem Khalaf Adyan Ali Noaman
Noor Al-Huda Hassan Kazim
2025 A.D
Supervised by 1446 A.H
Dr: Ali Salman
 1_Introduction
Parathyroid hormone (PTH) is a endocrine regulator responsible for
maintaining calcium and phosphate levels in the body. It plays a vital role
in bone metabolism, muscle contraction, nerve function, and blood
clotting. Importantly, it also influences the development and health of
dental tissues and jawbones. Disorders in PTH secretion—whether excess
(hyperparathyroidism) or deficiency (hypoparathyroidism)—can result in
systemic disturbances and oral complications that are detectable through
.clinical and radiological examinations

Intermittent Administration
Continuous Exposure
The impact of PTH on Dental Tissues
The parathyroid hormone (PTH) plays a crucial role in the remodeling of alveolar bone, which
is a key component of the periodontium that supports teeth. PTH influences bone density and
structure, meaning that fluctuations in its levels can significantly impact tooth stability and overall
oral health
Additionally, PTH regulates periodontal ligament cells and cementoblasts, both of which are
.essential for tooth attachment and function
Effects of PTH Disorders on Oral Health
Disorders of PTH secretion, such as hyperparathyroidism, can lead to significant oral manifestations.
Patients with primary hyperparathyroidism often experience decreased cortical bone density and may
.develop oral tori, which are bony overgrowths in the oral cavity

Therapeutic Applications of PTH

PTH analogs have been explored for their ability to enhance bone regeneration
within the oral cavity. Clinical studies have shown that teriparatide, a recombinant
form of PTH, can improve clinical outcomes in patients with periodontal defects by
.stimulating alveolar bone regeneration
2_Parathyroid gland
The parathyroid glands are small endocrine structures located
posterior to the thyroid gland, typically numbering four, though
variations can occur. Each gland measures approximately 5 mm × 3
mm × 1 mm and weighs between 35–40 mg . They are oval or bean-
shaped and play a crucial role in calcium homeostasis by secreting
parathyroid hormone (PTH)

2.1 Embryology and anatomical variations

The superior parathyroid glands originate from the fourth branchial pouch,
while the inferior glands derive from the third branchial pouch. During
embryonic development, the inferior glands descend with the thymus, leading
to their final position near the lower pole of the thyroid gland (Kluijfhout et al.,
2016). This migration can result in anatomical variations, with some individuals
having ectopic parathyroid tissue located in the mediastinum or within the
thyroid gland itself
2.2 Histology

The parathyroid glands are composed of two

main cell types :

Chief cells: Responsible for PTH synthesis and

secretion

Oxyphil cells: Increase in number with age and

have an unclear function but contain abundant
mitochondria, giving them an eosinophilic
cytoplasm
 2.3 Physiological Role of Parathyroid Hormone (PTH)

PTH is essential for maintaining serum calcium levels, acting on the

bones, kidneys, and intestines:

BONES KIDNEYS INTESTINES

Indirectly stimulates Enhances calcium Stimulates the
osteoclast activity, leading reabsorption in the distal conversion of vitamin D
to bone resorption and convoluted tubules. into its active form (1,25-
calcium release into the dihydroxyvitamin D),
bloodstream Inhibits phosphate which increases calcium
reabsorption in the absorption in the
. proximal tubules intestines
2.4 Regulations of PTH Secretion
PTH secretion is controlled by a negative feedback mechanism based on serum
calcium levels :

Low calcium levels reduce the activity of calcium-sensing receptors (CaSR) in chief cells,
leading to increased PTH secretion

Vitamin D also regulates PTH by inhibiting PTH gene expression

High calcium levels activate CaSR, suppressing PTH release

hyperparathyroidism
Hyperparathyroidism results from excessive PTH secretion, leading to
hypercalcemia. It is classified into :
Primary hyperparathyroidism: Often caused by a benign adenoma, leading to
excess PTH secretion
Secondary hyperparathyroidism: Results from chronic hypocalcemia due to
renal failure or vitamin D deficiency, leading to parathyroid gland hyperplasia
Tertiary hyperparathyroidism: Occurs when the glands become
autonomously overactive after prolonged secondary hyperparathyroidism
 HYPERPARATHYROIDISM

1_ parathyroid gland 2_thyroid gland

Hypoparathyroidism

Hypoparathyroidism is characterized by
insufficient PTH production, leading to
hypocalcemia. It is most commonly caused by
accidental removal or damage to the
parathyroid glands during thyroid or neck
,surgery. Symptoms include muscle cramps
tetany (involuntary muscle contractions), and
seizures. Treatment involves calcium and active
vitamin D supplementation
 2.6 Diagnostic Imaging and Surgical
Considerations

Accurate localization of parathyroid lesions is essential for

surgical planning, particularly in hyperparathyroidism
cases. Common imaging techniques include :

Ultrasonography

Sestamibi scan

-Four-dimensional computed tomography (4D

Parathyroid 4D CT image
)CT
Intraoperative PTH level monitoring helps confirm the successful removal
of hyperfunctioning parathyroid tissue, reducing the risk of persistent or
recurrent disease
 2.7 Recent Advanced and Future
Directions

Recent advancements in molecular imaging and minimally invasive surgery

have improved the management of parathyroid disorders. Near-infrared
autofluorescence (NIRAF) imaging has emerged as a promising technique
for real-time identification of parathyroid tissue during surgery, minimizing
the risk of accidental gland removal or damage

Additionally, research into the genetic basis of parathyroid diseases, such as

identifying mutations linked to familial hyperparathyroidism, is paving the way
for targeted therapies and personalized treatment strategies
3. Physiology of the parathyroid glands and the effects of hyperparathyroidism
and hypoparathyroidism

What are the parathyroid glands?

The parathyroid glands are four small endocrine glands located behind the thyroid gland.
Their main job is to regulate calcium and phosphate levels in the body by producing a
hormone called parathyroid hormone (PTH).

Why is calcium important?

Calcium plays a vital role in several body functions, including:

Muscle contraction (including the heart).

Nerve signal transmission.
Blood clotting.
Bone growth and strength.

Because of this, it’s important for the body to keep calcium

levels stable.
How do the parathyroid glands respond
to calcium levels?
The glands use calcium-sensing receptors (CaSR) to
detect the level of calcium in the blood:

When calcium levels drop:

The glands release more PTH.
PTH helps:
Release calcium from bones.
Reduce calcium loss through urine by
increasing kidney reabsorption.
Increase calcium absorption from food in
the intestines by activating vitamin D
(calcitriol).

When calcium levels are high:

PTH secretion decreases to avoid too much
calcium in the blood (hypercalcemia).
 3.1 Hyperparathyroidism

Hyperparathyroidism is a condition where the parathyroid glands produce too

much parathyroid hormone (PTH). This leads to high levels of calcium in the
blood (called hypercalcemia).

There are three types of hyperparathyroidism:

1. Primary Hyperparathyroidism:

Most common cause: A benign tumor (adenoma) in one of the parathyroid glands.
This causes uncontrolled PTH secretion, regardless of the calcium level.
Effects:
Increased calcium release from bones → leads to bone loss.
Less calcium excreted by kidneys→ builds up in the blood.
More calcium absorbed from the gut.
Result: bone weakening, kidney stones, and systemic health problems.
2. Secondary Hyperparathyroidism: 3. Tertiary Hyperparathyroidism:

Happens as a response to low calcium

levels in the blood (hypocalcemia). Occurs when the glands become
Common causes: overactive on their own, even after
Chronic kidney disease (CKD). the calcium levels are corrected.
Vitamin D deficiency. The glands no longer respond
Calcium malabsorption. properly to feedback and keep
producing excess PTH.
The body tries to compensate by
producing more PTH.
Long-term stimulation may cause
enlargement (hyperplasia) of the
glands.
Symptoms and Complications:

1-Skeletal issues:
• Osteoporosis.
• Increased risk of bone fractures.
• A condition called osteitis fibrosa cystica (due to overactive bone breakdown).
2-Kidney issues:
• Kidney stones due to excess calcium.
• Calcium deposits in the kidneys (nephrocalcinosis), which can lead to kidney failure.
3-Neuromuscular and mental symptoms:
• Fatigue, muscle weakness.
• Depression, memory problems, poor concentration.
4-Digestive symptoms:
• Nausea, constipation.
• Stomach ulcers due to increased acid secretion.
5-In severe cases:
• Hypercalcemic crisis, with symptoms like dehydration, confusion, heart arrhythmias, and
multiple organ failure—this is a medical emergency.
 3.2 Hypoparathyroidism

Hypoparathyroidism is a condition where the parathyroid glands produce too little

parathyroid hormone (PTH). This leads to low levels of calcium in the blood,
known as hypocalcemia.
Causes:
1. Most common cause:
Surgical removal or accidental damage to the parathyroid glands during
thyroid or neck surgeries.

2. Other causes include:

Autoimmune diseases.
Genetic disorders.
Magnesium deficiency, which interferes with PTH release.

Why Calcium Matters:

Calcium is essential for nerve signals, muscle movement, heart rhythm, and
bone strength. Without enough calcium, the body experiences serious
problems.
Symptoms and Complications:
Neuromuscular Symptoms:
Muscle cramps and painful spasms (tetany).
Tingling or numbness in the hands and feet (paresthesia).
Seizures in severe cases.
Breathing Difficulties
Laryngospasm (spasms in the throat), which can make breathing difficult and be life-
threatening.
Heart Problems:
Prolonged QT interval on ECG, which increases the risk of arrhythmias (irregular heartbeat).
Mental and Emotional Symptoms:
Anxiety, depression, confusion, memory issues — due to calcium’s role in brain function.
Long-Term Effects:
Dental defects.
Brittle nails.
Cataracts (clouding of the eye lens).
Dry skin — because calcium is vital for healthy tissues.
 condition Blood calcium level Main issues

Bone loss,kidney
Hyperparathyroidism High(Hypercalcemia)
stones,muscle weakness

cramps, heart
Hypoparathyroidism low(hypocalcemia)
problems,nerve symptoms
4. Signs and Symptoms of Hyperparathyroidism and Hypoparathyroidism

The parathyroid glands regulate calcium and phosphate levels in the

body through the secretion of parathyroid hormone (PTH).
Any disruption—either excess or deficiency of PTH—can affect many
body systems including:
• Skeletal system (bones)
• Kidneys
• Muscles and nerves (neuromuscular)
• Digestive system (gastrointestinal)
• Heart and blood vessels (cardiovascular)
 4.1 Hyperparathyroidism (HPT)
Common Signs and Symptoms:

1. Skeletal (Bones): 4. Digestive (GI):

Bone pain Constipation
Osteoporosis (bone thinning) Nausea
High risk of fractures Stomach ulcers and abdominal pain
(PTH takes calcium from bones, weakening (High calcium increases stomach acid)
them)
5. Cardiovascular (Heart & Vessels):
2. Kidneys:
High blood pressure (hypertension)
Kidney stones (from excess calcium)
Irregular heartbeats (arrhythmias)
Calcium buildup in kidney tissue
Calcium deposits in blood vessels
→
(nephrocalcinosis)
Can cause chronic kidney problems
→ Increases risk of heart attack and stroke

3. Neuromuscular (Nerves and Muscles): 6. Hypercalcemic Crisis (Severe Case):

Muscle weakness A medical emergency
Fatigue Includes:
Depression, poor memory, and confusion Dehydration
(Because high calcium affects how nerves Confusion or coma
work) Heart failure or cardiac arrest
4.2 Hypoparathyroidism (HypoPT)
Symptoms and Complications

1. Neuromuscular symptoms:

01 Tetany (involuntary, painful muscle contractions)

Muscle cramps
Paresthesia (tingling in the hands, feet, and face)
Carpopedal spasms (involuntary tightening of hands and feet)

2. Severe respiratory issues:

02 Laryngospasm (spasm of the throat muscles), which can cause breathing

difficulty or airway blockage

3. Cardiovascular symptoms:

03 Prolonged QT interval on ECG, increasing the risk of dangerous heart

arrhythmias

4. Neuropsychiatric symptoms:

04 Anxiety, depression, confusion, and memory problems due to calcium’s

role in brain function
 Long-term effects of chronic hypocalcemia:
Dental issues:
Delayed tooth eruption
Enamel hypoplasia (thin or underdeveloped enamel)
Brittle or weak teeth

Other tissue effects:

Dry skin
Brittle nails
Cataracts (clouding of the eye lens)
Parathyroid Surgery /(Parathyroidectomy)
Hair loss

Management and Treatment:

Hyperparathyroidism is often treated with parathyroidectomy (surgical removal of the overactive
gland).
Hypoparathyroidism is managed with:
Calcium supplements
Active vitamin D (calcitriol)
Newer treatments like PTH analogs are being developed and used, especially for patients with
long-term hypoparathyroidism.
 5. Oral Manifestations of Hyperparathyroidism and
Hypoparathyroidism

The parathyroid glands regulate calcium and phosphate levels, which

directly affect the oral cavity, including:

Teeth
Jawbones
Periodontal tissues (gums and bone)
Oral soft tissues

When PTH secretion is abnormal (too much or too little), it can lead to
oral complications, which may even appear before systemic symptoms
—making early detection by dentists very important.
5.1 Oral Manifestations of Hyperparathyroidism (HPT)

Hyperparathyroidism involves excess secretion of PTH, causing:

High blood calcium levels (hypercalcemia)

Increased bone resorption (breakdown)

These changes affect the oral and facial bones, often appearing as early signs of systemic disease.

5.1.1 Jawbone Changes and Bone Resorption

One of the most noticeable oral signs is jawbone demineralization.
This is due to increased osteoclast activity (cells that break down bone).
Key findings:
Loss of lamina dura (a white line around tooth roots seen in X-rays)
Generalized bone loss in the upper and lower jaws

This can cause:

Loose teeth
Misalignment of the bite (malocclusion)
Tooth mobility
Jaw fractures in severe cases
Figure . Panoramic radiograph of the skull shows well-circumscribed
bilateral radiolucency (arrows). There is maxillary bone loss and
diminished lamina dura. Loss of trabeculation and generalized and
ground glass appearance in the mandible is evident. The mandibular
canal (M) and cortical borders (C) are identifiable.
5.1.2 Brown Tumors (Osteitis Fibrosa Cystica)

Brown tumors are non-cancerous bone lesions

caused by long-standing hyperparathyroidism.
They form when bone resorption is extreme, and
fibrous tissue takes over.
In radiographs, they appear radiolucent (dark)
and may resemble cysts or tumors.
Clinical symptoms may include:
Facial swelling
Asymmetry
Localized pain
Difficulty in jaw function or biting
Facial asymmetry caused by brown tumors
 5.1.3 Periodontal and Dental Changes 5.1.4 Soft Tissue and Salivary Gland Dysfunction

Due to the effects of hypercalcemia on soft and hard tissues: Changes in the soft tissues may include:
Calcifications in the oral mucosa
Patients often have: Dry mouth (xerostomia) due to decreased saliva
Gum inflammation (gingivitis) Calcium deposits in salivary glands → may lead
Periodontal disease to salivary stones (sialolithiasis)
Loss of bone support around the teeth
Additional symptoms:
This can lead to: Burning sensation in the mouth
Loose teeth More frequent oral infections
Early tooth loss Delayed or impaired wound healing

In chronic cases, abnormalities may include:

Enamel hypoplasia (thin or underdeveloped enamel) xerostomia (dry mouth)
Abnormal dentin formation, weakening the tooth
structure
 5.2 Oral Manifestations of Hypoparathyroidism (HypoPT)
One of the most common dental signs is enamel
5.2.1 Dental Abnormalities hypoplasia:
This means the outer layer of the teeth (enamel) is
thin or underdeveloped.
It causes:
Increased cavities
Tooth sensitivity
Chipping and fractures
Other effects:
Poorly mineralized dentin
Defective cementum (the layer covering tooth roots)
Delayed eruption of baby and adult teeth
In severe cases:
Short and blunted roots
Very thin enamel layers
Early tooth loss
5.2.2 Increased Risk of Dental Caries and Pulp Calcifications

• Because of weak enamel and dentin, patients are more

prone to:
• Tooth decay (caries)
• Pulp calcifications (calcium deposits inside the tooth’s
nerve chamber) are common in chronic hypocalcemia:
• Seen on X-rays as white (radiopaque) areas
• Can lead to:
• Tooth pain
• Nerve death (pulpal necrosis) Intraoral periapical
• Difficulty during root canal treatments image show pulp
calcification (arrow)
 5.2.3 Jawbone and Periodontal Changes

Unlike hyperparathyroidism, which causes bone loss,

hypoparathyroidism causes increased bone density.
On radiographs, you may see:
Thickened cortical bone
More prominent bone patterns (trabeculation)
Retained baby teeth

Gum health (periodontium):

Delayed healing after dental procedures
Higher risk of gum infections
These issues can make dental treatment more complicated
 5.2.4 Oral Soft Tissue Changes
Due to low calcium affecting nerves, patients often feel:
Tingling
Numbness
Paresthesia (pins and needles) — especially in the lips
and tongue

Other soft tissue problems include:

Dry mouth (xerostomia)
Oral yeast infections (candidiasis)
Angular cheilitis (painful cracks at the corners of the
mouth)
Oral yeast infections These result from salivary gland dysfunction caused by
(candidiasis) calcium imbalance
6. Radiological Findings in Hyperparathyroidism and Hypoparathyroidism

Radiological imaging (like X-rays, CT, MRI, ultrasound, nuclear scans) is extremely helpful
in diagnosing and managing parathyroid disorders.
Because parathyroid hormone (PTH) affects calcium and phosphate, abnormalities show up
in the bones, teeth, and soft tissues.

6.1 Radiological Findings in Hyperparathyroidism (HPT)

In hyperparathyroidism, excess PTH causes bone loss, osteopenia, and calcium
deposits in soft tissues.

6.1.1 Skeletal Changes and Bone Demineralization

Common X-ray findings:
Generalized bone loss (osteopenia)
Weakened bones in the skull, spine, long bones, and jaw
Subperiosteal bone resorption (especially in fingers) — a classic sign of primary HPT
Thin cortical bone and rough bone texture (trabecular coarsening)

These changes make bones more prone to fractures

 6.1.2 Brown Tumors (Osteitis Fibrosa Cystica)

Brown tumors are non-cancerous bone lesions from

extreme bone resorption
On X-rays or CT scans, they appear as:
Radiolucent (dark), well-defined holes in bones
Seen in jawbones, long bones, and ribs

They form from overactive osteoclasts, fibrous tissue, and

bleeding inside the bone

Panoramic view of primary

hyperparathyroidism with
brown tumor of the mandible
6.1.3 Skull and Jaw Changes
• Skull X-rays may show a “salt-and-pepper” appearance:
• Due to bone resorption and porous areas
• Mandible (lower jaw) X-rays may reveal:
• Thinning of lamina dura
• Cortical bone loss
• Widened periodontal ligament space
• These changes contribute to loose teeth and malocclusion
Salt and paper sign(skull )

6.1.4 Renal and Soft Tissue Calcifications

Calcium deposits often build up in:

→
Kidneys seen as nephrocalcinosis on ultrasound or CT
Blood vessels, joints, and soft tissues

In severe cases, deposits may occur in the lungs, heart

muscle, or other organs, affecting their function

CT image show nephrocalcinosis

6.2 Radiological Findings in Hypoparathyroidism
(HypoPT)
In hypoparathyroidism, low PTH leads to hypocalcemia,
which causes:
Increased bone density
Abnormal dental development
Unusual calcifications in soft tissues and brain

6.2.1 Increased Bone Density and Sclerosis

Opposite of hyperparathyroidism:
Bones appear more dense (osteosclerosis) on X-rays

Skull, spine, and long bones show:

Thicker cortical bone
Panoramic view show symmetrical and
diffused bony sclerosis in the jaws
Prominent bone patterns (trabeculae)

In some cases, bones resemble osteopetrosis (stone bone

disease)
6.2.2 Dental and Jaw Abnormalities
Dental X-rays may reveal: These can cause:
Enamel hypoplasia Tooth pain
Poor dentin mineralization Pulp death (necrosis)
Delayed tooth eruption Complications during root canal
Pulp calcifications (seen as white masses treatment
inside tooth pulp)

6.2.3 Intracranial and Basal Ganglia Calcifications

A major finding in chronic Can lead to: CT image of basal

hypoparathyroidism: Movement disorders ganglia calcification
Calcium deposits in the brain — Seizures
especially in basal ganglia, Cognitive problems
cerebellum, and thalamus
Seen on CT scans
6.2.4 Soft Tissue and Vascular
Calcifications
Calcium can deposit in:
Tendons
Ligaments
Cartilage (a condition called chondrocalcinosis,
especially in knees and shoulders)

These are caused by long-term imbalances in

calcium and phosphate

Radiology provides critical clues that help in early

diagnosis and effective management of parathyroid MSK image show chondrocalcinosis
disorders. of knee cartilage
7. Diagnosis of Hyperparathyroidism and Hypoparathyroidism

Proper diagnosis is essential to manage symptoms effectively and

prevent complications.
Since both conditions affect calcium and phosphate metabolism,
diagnosis involves:

Clinical evaluation
Laboratory (biochemical) tests
Radiological imaging
Genetic testing (in some cases)

Differentiation is key:
It’s crucial to distinguish between:

Primary, secondary, and tertiary hyperparathyroidism

And between true hypoparathyroidism and other causes of low
calcium, like pseudohypoparathyroidism (when PTH is present but
ineffective).
7.1 Biochemical and Laboratory Diagnosis

7.1.1 Hyperparathyroidism
In hyperparathyroidism, PTH levels are too high, leading to high calcium and low
phosphate.
Typical lab findings include:
• High blood calcium
• Usually >10.5 mg/dL
• High or inappropriately normal PTH
• Confirms primary hyperparathyroidism
• Helps rule out other causes of high calcium
• Low blood phosphate
• <2.5 mg/dL, due to increased phosphate loss in urine
• Elevated active vitamin D (1,25-dihydroxyvitamin D)
• PTH stimulates the kidney to activate vitamin D
• High calcium in the urine (hypercalciuria)
• Common in primary HPT and may lead to kidney stones
 7.1.2 Hypoparathyroidism

In hypoparathyroidism, there is not enough PTH, causing low calcium and high phosphate.
Typical lab findings include:

Low blood calcium

<8.5 mg/dL, due to reduced PTH

Low or undetectable PTH

Differentiates it from pseudohypoparathyroidism (where PTH is high, but doesn’t work)

High blood phosphate

>4.5 mg/dL, since PTH usually helps remove phosphate through urine

Low active vitamin D (1,25-dihydroxyvitamin D)

Because PTH is needed to activate vitamin D in the kidneys

Low urine calcium

Unlike in hyperparathyroidism where calcium in the urine is high
 Lab Marker Hyperparathyroidism Hypoparathyroidism

Serum Calcium High(>10.5 mg/dL) Low(<8.5 mg/dL)

PTH High or inappropriately normal Low or undetecte

Serum Phosphate Low High

Active Vitamin D High Low

Urine Calcium High (kidney stone risk) Low

 7.2 Radiological and Imaging Diagnosis

Imaging is essential in diagnosing parathyroid disorders, especially:

When patients have no symptoms

Or when parathyroid tumors or abnormalities are suspected

7.2.1 Ultrasound
Neck ultrasound is the first-line imaging technique for
detecting:
Parathyroid adenomas (benign tumors)
Parathyroid hyperplasia (gland enlargement)

On ultrasound:u
Enlarged parathyroid glands appear dark (hypoechoic)
Ultrasound scan of
Advantages: parathyroid adenoma
Non-invasive, quick, and no radiation exposure
7.2.2 Sestamibi Scan (99mTc-Sestamibi)
A nuclear medicine scan used to
locate overactive parathyroid
glands, especially in primary
hyperparathyroidism

The radiotracer (technetium-99m)

is taken up by hyperfunctioning
adenomas

The overactive gland lights up

clearly on gamma camera images

Very sensitive: over 85% accuracy

in detecting parathyroid
adenomas
7.2.3 CT and MRI Scans

4D-CT scans provide highly detailed anatomical images and are used
when:
Ultrasound and sestamibi scans are inconclusive

CT helps detect:
Calcified tumors
Ectopic (misplaced) parathyroid glands
Hyperplasia (gland overgrowth)

MRI is useful for: CT Scan of the neck suggests

Detecting parathyroid cancer parathyroid hyperplasia

Assessing vascular invasion (if malignancy is suspected)

7.2.4 Bone Densitometry (DEXA Scan)

DEXA is used to measure bone mineral density (BMD) in patients with

hyperparathyroidism
Common findings include:
Osteoporosis
Cortical bone thinning
Loss of trabecular bone

Most affected areas:

Spine
Femoral neck (hip)
Radius (forearm)
7.2.5 Skull and Jaw Radiographs

In hyperparathyroidism, X-rays may show:

Subperiosteal bone resorption
A “salt-and-pepper” appearance of the skull
Brown tumors in the jaw

In hypoparathyroidism, X-rays may show:

Thickened cortical bones
Pulp calcifications (calcium buildup inside tooth pulp)
Delayed tooth eruption
 7.3 Genetic Testing for Hereditary Parathyroid Disorders

In some cases, parathyroid disorders are inherited, meaning they run in families.
When a genetic cause is suspected, genetic testing is important to:

Differentiate familial (inherited) hyperparathyroidism from sporadic (random)

cases
Identify if the patient has a hereditary syndrome that may affect multiple glands
or organs

When is genetic testing recommended?

Genetic testing is especially useful in:

Young patients diagnosed with parathyroid problems
Patients with recurring parathyroid disease after treatment
People with a family history of endocrine tumors (hormone-producing tumors)
Common genes involved in hereditary
parathyroid disorders:
1.CDC73 (also known as HRPT2):
1. MEN1 (Multiple Endocrine Neoplasia type 1):

A syndrome where tumors can Linked to hyperparathyroidism-

occur in the parathyroid jaw tumor syndrome
glands, pancreas, and pituitary Patients may develop parathyroid
gland tumors and jaw tumors

1.CASR (Calcium-Sensing Receptor gene):

Mutations here affect the body’s

ability to regulate calcium
Can lead to abnormal calcium levels
and PTH secretion problems
Why is genetic testing important?

• Helps diagnose hereditary conditions early

• Guides treatment planning
• Informs family members about their genetic risks
• Supports long-term monitoring for other associated
endocrine issues
8. Integration of Parathyroid Hormone (PTH) Function
and Its Impact on the Oral Cavity
Overview:

The parathyroid glands play a key role in calcium and

phosphate balance, which is essential for:
• Bone metabolism
• Tooth development
• Periodontal health (gums and jawbones)

Any disruption in PTH secretion — whether too much

(hyperparathyroidism) or too little (hypoparathyroidism)
— can lead to oral and systemic issues that are detectable
through:
• Blood tests
• Radiographic imaging
• Clinical examination
 8.1 PHYSIOLOGY OF THE PARATHYROID
GLANDS AND ORAL RELEVANCE

PTH helps regulate:

Calcium levels in blood by acting on:

Bones (releasing calcium)
Kidneys (reducing calcium loss)
Intestines (via activation of
vitamin D for calcium absorption)

These functions directly influence:

Jawbone density
Tooth mineralization
Gum and periodontal stability

Abnormal PTH levels lead to changes in

oral structures and bone health.
 8.2 Hyperparathyroidism: Systemic and Oral
Consequences

Excess PTH secretion results in: Radiographic signs:

Hypercalcemia (high blood
calcium) Subperiosteal bone resorption
Bone resorption (loss) Brown tumors
Loss of lamina dura (thin bone
Oral effects include: lining around teeth roots)

Jawbone demineralization
Tooth mobility Dentists may detect these signs early —
Periodontal disease even before general symptoms appear.
 8.3 Hypoparathyroidism and Dental Impact

Low PTH levels cause:

• Hypocalcemia (low calcium)

Dental effects include:

• Enamel hypoplasia (weak outer tooth layer)
• Delayed tooth eruption
• Pulp calcifications
• Brittle teeth and increased sensitivity

Enamel hypoplasia has affected

Neuromuscular effects (due to low calcium):
the dentition of this patient,
• Tetany (muscle spasms) who had hypoparathyroidism
• Paresthesia (tingling) while the teeth were forming.
• Difficulty speaking and swallowing

These increase the risk of caries and periodontal disease,

requiring early dental care.
 8.4 Radiological Findings: Early Detection through Imaging

Radiographs are key to spotting parathyroid-related skeletal changes.

In hyperparathyroidism:
General bone loss
Thinning of cortical bone
Brown tumors
Widened periodontal ligament space

In hypoparathyroidism:
Increased bone density
Pulp calcifications
Delayed tooth development

Dental imaging is a powerful tool for detecting endocrine disorders early

8.5 Diagnosis: Combining Blood Tests and Oral Exams
Diagnosis relies on:

Biochemical tests:
Hyperparathyroidism: high calcium, high PTH
Hypoparathyroidism: low calcium, high phosphate, low PTH

Imaging (Ultrasound, Sestamibi, CT, MRI) for localizing tumors

Oral examinations for early dental signs of systemic disease
 8.6 Clinical Implications and Future Perspectives

Collaboration between:

Dentists
Endocrinologists
Radiologists
is essential for early detection and management.

New treatment options include:

PTH analogs (for chronic hypoparathyroidism)

Targeted gene therapy (for inherited forms and complex cases)

These innovations may reduce long-term dental and bone complications.

 Thank you for
your attention
2024/2025