• Two pairs of glands
• Behind the left and right lobes of the thyroid
• About 6 mm long and 3 to 4 mm wide, and 1
to 2 mm anteroposteriorly
• Chief cells- synthesize and release parathyroid
• Single chain polypeptide -84 a.a
– Single adenoma- MC
– Multiple adenomas
– Nodular hyperplasia
– chronic renal insufficiency.
– Osteomalacia & rickets
• Hyperparathyroidism may result in either bone resorption or bone
formation, bone resorption usually dominates.
• Normal values are 10 to 55 pg/ml
• Both sexes affected
• 2-3> women
• Middle aged
o Bones, stones, abdominal groans, psychic
Radiologic findings of
• The M/C radiologic abnormality is generalized osteopenia.
• Bone resorption, bone sclerosis, brown tumors,
chondrocalcinosis, soft tissue calcification, and vascular
• Brown tumors appear as well-defined lytic lesions.
– After resection of parathyroid adenomas, the lesions may become
sclerotic and may mimic blastic metastasis.
– (Brown tumors are composed mostly of osteoclasts )
• Bone resorption, the most characteristic finding, is usually
– subchondral, trabecular, endosteal, intracortical, subperiosteal,
subligamentous, and subtendinous.
Radiologic findings of
• Subperiosteal resorption - M/C
– Usually occurs in the hands and feet.
– M/C affected site: radial aspects of the middle phalanges.
– Acro-osteolysis or phalangeal tufts resoption may also be present.
• Trabecular resorption
– Often seen in the diploic space of the skull, where it has a
characteristic salt and pepper appearance.
• Subchondral resorption
– May be seen in the sacroiliac joints, sternoclavicular joints,
acromioclavicular joints, symphysis pubis, and discovertebral
AP radiograph of the hand in a 66-year-old woman with primary hyperparathyroidism owing to
parathyroid adenoma shows subperiosteal bone resorption ( arrows) along the radial
aspect of 2nd, 3rd, and 4th middle phalanges.
AP radiograph of the knee in a child with hyperparathyroidism shows subperiosteal
bone resorption ( arrow) along the proximal medial tibia.
Lateral radiograph of the skull in a 23-year-old man with secondary hyperparathyroidism
shows trabecular resorption of the diploic space ("salt and pepper" appearance).
Dental radiograph in another child with hyperparathyroidism shows resorption (
arrow) of the lamina dura of the mandible.
Radiologic findings of
• Bony sclerosis; focal or
appearance of spine.
• Soft tissue and
• usually seen in the menisci of
the knee, the triangular
fibrocartilage of the wrist, and
the pubic symphysis
AP radiograph of the wrist in an 83-year-old woman with primary hyperparathyroidism shows
chondrocalcinosis ( arrow) of the triangular fibrocartilage.
Secondary HPT. Radiograph of the pelvis and hips showing diffuse osteosclerosis( coarse striations)
A, AP radiograph of the spine in a patient with secondary hyperparathyroidism shows generalized bone
sclerosis, small kidneys, and left renal calculi. B, Lateral radiograph of the lumbar spine in another
patient with secondary hyperparathyroidism shows horizontal, bandlike ("rugger jersey") sclerosis of
the vertebral bodies ( arrows).
AP radiograph of the hand in a 50-year-old man with renal osteodystrophy shows acro-osteolysis
( short arrows), subperiosteal bone resorption ( long arrows), and vascular calcifications.
Secondary HPT. Radiograph of the hand showing resorption of the first to third tufts with soft tissue
calcification (1). There is articular calcification (2), and subperiosteal and subligamentous resorption (3).
The differential diagnosis of
• Focal subperiosteal resorption involving a single bone
– Neoplasms or osteomyelitis.
• Bone sclerosis in patients with secondary
– Metastatic disease, radiation-induced bone disease,
hypoparathyroidism, myelofibrosis, mastocytosis, sickle-cell
disease, and Paget's disease.
– Pyrophosphate arthropathy (CPPD) or hemochromatosis.
• Brown tumors
– includes other focal lytic lesions, such as giant cell tumor and
• Osteoporosis – late onset, Ca++ -N
• Osteitis Deformans(Pagets disease)- Se Ca++ -
N, ALP , X ray- mainly pelvis, lumbar spine,
femora, skull involved, deformities r common
• Osteomalasia- Ca++ , ALP , response to
Vitamin D (+), X ray- bending of bones (+)
• Osteogeneis imperfecta- multiple fractures,
childhood disease, blue sclera.
1. Management of acute hypercalcemia by
rehydration with normal
2. Medical line : -Monitor serum creatinine levels
and calcium levels every 6 months.DEXA scan
on an annual basis.
-Avoid thiazide diuretics.
-Maintain high oral fluid intake.
-Improving bone mineral density and achieving
calcium homeostasis by calcimimetics and HRT.
3. Surgery : -Is indicated in patients with
complications and in younger age group.
-Minimally invasive surgery to excise
Subtotal parathyroidectomy in case of
diffuse hyperplasia are being done.
• It occurs when PTH secretion is increased to
compensate for prolonged hypocalcemia.
• It is seen in patients with chronic renal failure
where the failing kidneys do not convert
vitamin D to its active form and they do not
Excess phosphate combines with calcium to
form calcium phosphate.
• Both processes lead to hypocalcemia,cause
hyperplasia of all parathyroid tissue and hence
• Secondary hyperparathyroidism can also
result from malabsorption of vitamin D
due to chronic pancreatitis, small bowel
disease, bariatric surgery.
• CLINICAL FEATURES : are mostly of renal
failure. If it is due to vitamin D deficiency,
limb deformities, pathological fractures
• INVESTIGATIONS : Serum calcium levels are
low.PTH levels are raised. Phosphate levels depend
on etiology (e.g. high in renal disease, low in
vitamin D deficiency).
Radiology shows evidence of bone disease.
• TREATMENT : Medical line is the mainstay.
The underlying condition needs to be treated
-correcting vitamin D deficiency.
-treatment of chronic kidney disease
Treatment with vitamin D and its analogues.
• In a small proportion of cases of secondary
of the parathyroids results in adenoma
formation and unregulated PTH secretion.
• Even correction of the underlying cause will
not stop excess PTH secretion i.e parathyroid
gland hypertrophy becomes irreversible.
• CLINICAL FEATURES : Symptoms and signs are
due to hypercalcemia so presentation is similar
to primary hyperparathyroidism.
• INVESTIGATIONS : Serum calcium and PTH
levels are raised.
Phosphate levels are often high.
• TREATMENT : Total or subtotal
parathyroidectomy is the recommended
Autotransplantation of parathyroid tissue in the
forearm is also commonly carried out.