Generalized rarefaction of jaw bones /prosthodontic courses

GENERALIZED RAREFACTION
OF JAW BONES
WWW.INDIANDENTALACADEMY.COM
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education

• Bone is a complex organ consisting of dense outer
cortex covered by periosteum.
• Inner medullary portion consists of-marrow spaces, red
or yellow bone marrow.
• Inner surface of cortex is lined by endosteum
• Osteoblasts and osteoclasts are cells which regulate the
bone
• Osseous, endocrine, GIT, nutritional, renal,
haemopoietic systems are normally maintains the bone
density.

Hormones that promote the bone formation:
growth hormone
testosterone
oestrogen
calcotonin
Promote the resorption of bone:
PTH
cortisol
thyroxine

NORMAL VARIATIONS IN RADIODENSITY
 Men have heavier bones than women b/c the effects of
testosterone.
 Bone is denser in anterior man.
 with in physiological limits, the greater the mechanical
forces more r/o the image of the bone.

• Hyperparathyroidism
• Osteoporosis
• Osteomalacia
• Hereditary hemolytic
anemia
• Leukemia
• Langerhan’s cell disease
• Paget’s disease(early)
• Multiple myeloma(late)
• Rarities:
Agranulocytosis
Burkitt’s lymphoma
Diabetes
Down’syndrome
Gaucher’s disease
Hypophosphatemia
Multiple metastatic
carcinomas
Polycythemia
Progeria,rickets
CAUSES

HYPERPARATHYROIDISM
• It is an endocrine abnormality in which there is an
excess of PTH
• As a result it mobilizes calcium from skeleton and
increases renal tubular reabsorption of calcium,the net
result is increase in the serum calcium levels

• Three types
Primary, secondary, tertiary.
Primary:
• Result from a benign tumor of one of the parathyroid
gland
• the elevation of serum calcium levels and elevated serum
levels of PTH is a diagnostic of hyperparathyroism
• Incidence is about 0.1%

• Secondary:
• Results from compensatory increase in output of
PTH in response to hypocalcemia.
• Underlying hypocalcemia may be result from
inadequate dietary intake,or poor intestinal
absorption.
• Tertiary:
• Parathyroid tumours develops after long standing
secondary hyperparathyroidism.

Metastatic calcifications:
• ectopic calcifications is most common feature.
Subperiosteal erosions:
• Erosions of bone phalanges .
• Loss of laminadura is a type of subperiosteal erosion,
osteitis fibrosa generalisata(cystica):
• refers to pattern of generalised rarefaction of bone.
• Bones may appear quite r/l with thin cortices and hazy
indistinct trabeculae.
• Some may less homogenous produce moth eaten
appearance.

R/G FINDINGS LF JAWS:
• thinning of the cortical boundaries.
• Density of the jaws is decreased.
• The teeth stand out in contrast to the radiolucent jaws.
• The change in the normal trabecular pattern that is ground
glass appearance(granular)
• Sometimes mottled or moth eaten appearance.
• Partial or complete loss of lamina dura
• Trabeculae are numerous small randomly oriented .

BROWN GIANT CELL LESION
More common in sec hyperparathyroidism
Most common in mandibular molar area.
 Develops in 10% of patients.
• Most common in jaws may cause r/l s that are central or
peripheral and unilocular or multilocular.
• Unilocular: cyst like borders
borders indistinct
• Multilocular soap bubble appearance.
• the lesions may develop multiple with in a single bone.

D/D:
• Unilocular:
post extraction socket, Primordial bone cyst,
traumatic bone cyst, odontogenic cyst-Serum
chemistry is normal.
Multilocular:
Paget's disease, ameloblastoma, CGCG, Cherubism,
Fibrous dysplasia, multiple myeloma.

• Primary
hyperparathyroidism:
• inc level of serum
calcium.
• Serum phosphatase dec
• Serum alkaline
phosphatase inc.
• Secondary
hyperparathyroidism:
• Serum calcium levels
normal-decrease
• Serum phosphatase-inc
• Serum alkaline
phosphatase-inc
D/D OF PRIMARY AND SECONDARY:

R/G PICTURE OF HYPERPARATHYROIDISM-
GROUND GLASS APPEARANCE

R/G OF HPT-LOSS OF LAMINA DURA AND
GROUND GLASS PATTERN

GRANULAR BONE PATTERN

BROWN TUMOUR IN HYPERPARATHYROIDISM

BROWN TUMOUR IN MANDIBULAR ANTERIOR
REGION

Osteoporosis:
• Most common form of metabolic bone disorder, Decreasing bone
density, leading to fracture.
• Non specific reaction of skeleton to several factors or diseases.
• Resulting from primary deficiency of bone matrix with secondary
deficit of mineral.
• Imbalance b/n bone formation and bon eresorption.
• Occurs in 3 ways:
• A slight increase in bone resorption with a slight decrease in
formation.
• A severe increase in in bone resorption with a normal rate of
formation.
• normal bone resorption with a severe decrease in formation.

• Postmenopausal osteoporosis :
Decrease in PTH levels.
• Senile osteoporosis:
1-alfa hydroxylase are depressed.
• Cushing's syndrome
• Drug induced osteoporosis:
cortisol and cortisone
malnutritional status
Thyrotoxic osteoporosis

C/F:
• fracture
• bone pain
• most commonly postmenopausal woman
affected

R/G FINDINGS
• Must be a 30-60% of calcium content loss from bone can
be detected on r/gs.
• Dec in density of bone
• Loss of normal trabecular pattern and thinning of cortex.
• Generalized rarefaction of jaw bones.
• Individual trabeculae are fine and indistinct.
• Diffuse granularity
• Cortical borders are rhinner and less distinct
• Mandibular angular cortex –it is thinner in osteoporosis.

osteoporosis evident as a loss of the normal
thickness and density of the inferior cortex of the
mandible

Osteomalacia and rickets:
• Accumulation of osteoid in place of mineralized bone.
• Caused by deficiency of calcium
• Etiology:
vitamin deficiency
calcium malabsorption
liver and renal disorders
prolonged anticonvulsive drug therapy
hypophosphatemic rickets

• Result from defect in normal activity of metabolites of
vitamin d .
• Failure of normal activity of vitamin D may
occur as a result of the following:
1. Lack of vitamin D in the diet
2. Lack of absorption of vitamin D
3. Lack of metabolism of the active metabolite
1,25(OH) 2 D that is required for intestinal
absorption of calcium.

• Rickets:
• disease affects the growing children in infants and
children.
• Osteomalacia:
• disease affects mature skeleton in adults
clinical findings:
rickets:
Affects first 6months of life.
craniobates-a softening of posterior of parietal bones.
development of dentition is delayed.
eruption of teeth is retarded

osteomalacia:
• bone pain, muscle weakness,
• waddling or penguin gait.
• fractures
• Pseudofractures(milkman fractures), green stick
fractures
• tetany

R/G FINDINGS
• Generalized rarefaction
• Cortical thinning
• Homogenous granular appearance
• Lamina dura may be thin or less prominent.

RICKETS MAY CAUSE THINNING (HYPOPLASIA)
OR DECREASED MINERALIZATION
(HYPOCALCIFICATION) OF THE ENAMEL

osteomalacia may cause a loss of bone, resulting i n
an increased radiolucency of the alveolar bone and
lamina dura

HEREDITARY HAEMOLYTIC ANEMIAS
• Rarefaction is caused by development of larger than
usual marrow spaces, a greater ratio of medullary bone
to cortical bone.
• It is result of a marked hyperplasia of hematopoietic
tissue induced by increased demand for effective
erythrocytes in anemias.
• A fatty marrow of maxilla and mandible may revert to
hyperplastic hemopoietic variety in response to stress
induced by anemias.

THALASSEMIA(MEDITERRANEAN AND COOLEYS
ANEMIA)
• Defective erythrocyte with a deficient amount of
structurally normal hemoglobin.
Types:
• thalassemia major-
infants and children
Pallor, weakness, severe anemia, irritability, lethargy

• thalassemia minor-
asymptomatic
• intermediate thalassemia-
less severe
The face develops prominent cheekbones and a protrusive
premaxilla resulting in a "rodent-like" face

R/G FINDINGS
• result from hyperplasia of the ineffective bone marrow and
its subsequent failure to produce normal red cells.
• Skull is enlarged because of an increase in the width of
dipole
• Sometimes numerous white hair like shadows arising from
the inner table of cranial vault appear to protrude from the
surface of the bone and produce the hair on end
appereance.
• Maxilla, mandible, zygoma are markedly increased in size
and paranasal sinuses are decreased in size except
ethmoidal sinus b/c of lack of red bone marrow.

• Severe bone marrow hyperplasia prevents pneumatization
of the paranasal sinuses, especially the maxillary sinus, and
causes an expansion of the maxilla that results in
malocclusion.
 The jaws appear r/l, with thinning of the cortical borders
and enlargement of the marrow spaces.
• The trabeculae are large and coarse
• The lamina dura is thin, and the roots of the teeth may be
short.
• Occasionally honey comb pattern.

SICKLE CELL ANEMIA
• ‘Sickle cell anemia is an autosomal recessive,chronic,
hemolytic blood disorder.
• Patients with this disorder have abnormal hemoglobin
(deoxygenated hemoglobins),
which under low oxygen tension results in sickling of
the red blood cells.
 The hemopoietic system responds to resultant anemia by
increasing production of RBC which requires
compensatory hyperplasia of the bone marrow.
.

Clinical findings:
 affects mostly children and adults.
 Milder: weakness, shortness of breath, fragility
 Crisis: severe abdominal, joint, muscle pain.
 heart murmers
 high temperature
 Circulatory collapse
 Weakness ,dyspnea, oral ulcers on gingiva
 splenomegaly

R/G FINDINGS
 thinning of trabeculae, and reduced in number
 remaining trebeculae appear coarsened and sharply
defined.
 Prominent horizontal trabeculae b/n the teeth have
stepladder pattern.
 Lamina dura is normal
 May be sclerotic areas in bone that represents healed
infracts.
 the skull may show widening of dipoliac space.
 Thinning of inferior border of mandible.

TRUE LATERAL SKULL SHOWING WIDENING OF THE DIPLOIC
SPACE AND THINNING OF THE INNER AND OUTER TABLES
AND EARLY HAIR-ON-END APPEARANCE ANTERIORLY
(ARROWED

PERIAPICAL SHOWING THE GENERALIZED
COARSE TRABECULAR PATTERN IN THE
MANDIBLE.

A.ENLARGED BONE MARROW SPACES IN THE MANDIBLE.
B, NORMAL MANDIBLE FOR COMPARISON

Skull showing the hair-on-end bone pattern.

LEUKEMIA
 It is a malignancy of the hematopoeitic tissue involving
one of the leukocytic cell types
C/F:
 Anemia
 Thrombocytopenia
 Tissues may be infilterated or infected by the
proliferating luekimic cells
 Pallor & weakness
 Petechiae or echimosis in the mucus membrane or skin

ORAL FINDINGS
• Gingival enlargement
• Bleeding
• Gangrenous stomatitis
• Lymphnode enlargement
• Hepatosplenomegaly
• Ulcers covered with yellowish grey pseudomembrane
that bleeds easily.
• Pallor
• Leukemic infiltration may produce swelling of palate.

R/F
• May vary from multiple punched out r/ls to
solitary, moderately well defined areas of
osteolysis to generalized rarefaction.
• Occasionally osteosclerosis

Worth:
• The formation of tooth crowns may be incomplete or delayed
• The cortices of the tooth crypts may be partially or completely
destroyed
• There may be enlargement of the tips with failure of the bone
formation above the apical portion of developing tooth
• Developing teeth may assume an asymmetric position within
the crypt with or without distruction of part of the crypt coretx
• Incompletely formed crowns may be situated entirely above the
alveolar crest being completely elevated out of the bone
• Partially formed teeth especially those having incomplete root
formation maay have succesfull rapid eruption

• Silverman- 3 types of r/g findings in leukemia
1.Most commonly-bone destruction in the form of
transverse lines of increased r/l at the end of the
long bones or irregular areas of bone loss(moth
eaten appearance)
2.Sclerosis-alone or in combination with
destruction.
3.Formaton of bone beneath the periosteum.

MULTIFOCAL AREAS OF BONE DESTRUCTION AND
WIDENING OF PORTIONS OF THE PERIODONTAL
LIGAMENT SPACE

panoramic radiograph of the patient. the
punched-out radiolucent lesions in the
mandible

LATERAL SKULL RADIOGRAPH OF THE PATIENT. ARROWS
INDICATE SOME OF THE PUNCHED-OUT RADIOLUCENT
LESIONS-CASE REPORT

LANGERHAN’S CELL DISEASE
• In 3 forms of LCH , most commonly acute disseminated form
produces generalized rarefaction.
• Bone destruction commences at the alveolar crest instead of
deep in to medullary region(leukemia)
• Extrusion of teeth, thinning of cortices, thinning of lamina
dura
• Involvement of crypt cortex
• Proliferative periosteitis (juvenile cases).

PAGET’S DISEASE
• The early stage of paget.s disease (radiolucent) may
cause a general homogenous rarefaction of jawbones and
fine fine, granular ground glass appearance.
• Maxilla is most commonly involved.
• Cortices are thinned and lamina dura is missing.

MULTIPLE MYELOMA
• In advanced cases gross destruction of medullary
portions of bones combined with resorption of cortices
may produces generalized rarefaction of jaw bones.

PANORAMIC RADIOGRAPH – RADIOLUCENT LESIONS IN
THE SYMPHYSIS, BODY AND MANDIBULAR LIMB.

DIFFERENTIAL DIAGNOSIS
Hyperparathyriodism:
• Subperiosteal erosions
• hypophospataemia
• Laboratory investigations
• Most commonly occur older individuals.
• Primary-hypercalcemia

Osteomalacia:
• pseudo fractures, green stick fractures
Langerhan’s cell disease:
Commences at the alveolar crest
Leukemia:
Originating from deeper portions of medullary bone.

• Thalassemia,sickle cell anemia, acute leukemia, Acute
dissiminated langerhans cell disease –Commonly occurs
in young individuals.
• Hyperparathyroidism, osteoporosis, osteomalacia, pagets
disease, multiple myeloma-commonly occurs in older
individuals.

REFERENCES:
 Principles practice oral radiologic
interpretation H.m worth
 Oral radiology principles and interpretation 5th
edition white & pharaoh
 Differential diagnosis of orol and maxillofacial
lesions 5th edition norman.k and wood,paul
w.goaz

Generalized rarefaction of jaw bones /prosthodontic courses

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (9)

Similar to Generalized rarefaction of jaw bones /prosthodontic courses

Similar to Generalized rarefaction of jaw bones /prosthodontic courses (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Generalized rarefaction of jaw bones /prosthodontic courses