Systemic Diseases Manifested in the Jaw.ppsx

8/10/2019 Systemic Diseases Manifested in the Jaw.ppsx

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By Naglaa S. El Kilani


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Because systemic disorders affect theentire body, the radiographic changesmanifested in the jaws are generalized.

The general changes include the following:1. A change in size and shape of the bone2. A change in the number, size, and

orientation of trabeculae

3. Altered thickness and density of corticalstructures4. An increase or decrease in overall bone

density

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Changes to teeth and associated structuresinclude the following:

1. Accelerated or delayed eruption2. Hypoplasia3. Hypocalcification4. Loss of a distinct lamina dura

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Parathyroid function:Parathyroid hormone

preserves blood

calciumby several

major effects: Enhancing absorption

of calcium from the

small intestine

Suppression of calciumloss in urine

Mobilization of calcium

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Evidence in the jawsof: - Osteopenia (in mandible and maxilla)

producing a very fine trabecular pattern (ground glass)

- Loss of the lamina dura surrounding all theteeth

Thinning or loss of the normal thick corticalbone of the lower border of the mandible

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Hyperpituitarism results from

hyperfunction of the anterior lobe of the

pituitary gland, which increases theproduction of growth hormone.

Classification:

1. Gigantism ( before puberty)2. Acromegaly (after puberty)

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This is a disturbance of bone growthcaused by hypersecretion of growthhormone(GH) usually as the result of apituitary adenoma developing afterpuberty.

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Radiographic Features

In infants:

Early eruption of the primary teeth Premature loss.

In adults :

A generalized decrease in bone density.

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Cushing's syndrome arises from an excess ofsecretion of glucocorticoidsby the adrenal

glands.

The increased level of glucocorticoid resultsin a loss of bone mass from reducedosteoblastic function and either directly orindirectly increased osteoclastic function

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Clinical Features Females three to five more than males. Usually seen in the third or fourth decade. Often show obesity (which spares the

extremities). kyphosis of the thoracic spine "buffalo

hump" Muscle Weakness Hypertension Concurrent diabetes.

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Normally bone remodeling processes are tightly coordinated

Osteoporosis occurs when bone resorption exceedsformation.

Collagen as well as mineral is lost from bone resulting in ageneralized decrease in bone mass.


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Occurs with the aging process of bone

Bone mass normally increases frominfancy to about 35 to 40 years of age.

At this time there begins a gradual and

progressive decline, occurring at the rateof about 8% per decade in women and 3%per decade in men.

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Secondary osteoporosis: Nutritional deficiencies

Hormonal imbalance Inactivity Corticosteroid Heparin therapy.

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Clinical Features Postmenopausal women.

Fracture. The most common locations are the distal

radius, proximal femur, ribs, and vertebrae. Bone pain.

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Radiographic Features An overall reduction in the density of bone.

Thinning of cortical boundaries such as theinferior mandibular cortex. Accurate assessment of bone mass loss is

difficult but may be done with dual energyphoton absorption (DEXA) or quantitativecomputed tomography (QCT) programs.

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They result from inadequate serum andextracellular levels of calcium and phosphate

minerals.

Both abnormalities result from a defect inthe normal activity of the metabolites ofvitamin D, especially 1,25(OH)2D, required forresorption of calcium in the intestine.

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Such defect may occur due to: 1. Lack of exposure to ultraviolet light required

for conversion of provitamin D3

2. Lack of conversion of vitamin D3 to 25(OH)Din the liver.

3. Lack of metabolism of 25(OH)D2 to1,25(OH)2D by the kidney .

4. A defect in the intestinal target cell responseto 1,25(OH)2D or inadequate calcium supply.

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Clinical Features Rickets:

In the first 6 months of life: Tetany or convulsions resulting from the

hypocalcemia of rickets.Later in infancy: Deformity of the extremities. Delayed development of the dentition Retarded eruption rate of the teeth.

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Osteomalacia: Bone pain.

Muscle weakness of varying severity. Peculiar waddling or "penguin" gait, Tetany Bone fractures.

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Radiographic Features General radiographic features:

In rickets: A characteristic bowing of the femur and tibia. Greenstick fractures (an incomplete fracture).In osteomalacia: T he cortex of bone may be thin. Pseudofractures may also be present

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Radiographic features of the jaws: Within the cancellous portion of the jaws, the

trabeculae become reduced in density, number,and thickness.

Radiographic changes associated with the teeth: In Rickets :Hypoplasia of developing dental

enamel.

The lamina dura and the cortical boundary oftooth follicles may be thin or missing.

Osteomalaciadoes not alter the teeth

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Osteopetrosis is a disorder of bone that results from adefect in the differentiation and function ofosteoclasts.

The lack of normally functioning osteoclasts results inabnormal formation of the primary skeleton and a

generalized increase in bone mass.

Obliteration of the marrow compromises

hematopoiesis and compresses cranial nerves.

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Clinical Features Progressive loss of the bone marrow .

A severe increase in bone density. Hydrocephalus Blindness, deafness, vestibular nerve

dysfunction, and facial nerve paralysis. Bone pain . Osteomyelitis that is more common in the

mandible.

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Radiographic FeaturesGeneral radiographic features: Increased bones density, which is bilaterally

symmetric. The trabecular patterns of the medullary cavity

may not be visible.Radiographic features of the jaws:

The increased radiopacity of the jaws so thateven the roots of the teeth may not beapparent.

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Radiographic features associated with theteeth:

Delayed eruption, early tooth loss, missingteeth, malformed roots and crowns. The lamina dura and cortical borders may

appear thicker than normal.

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Sickle cell anaemia Thalassaemia (Cooley'sanaemia)

Hereditary, chronic, haemolyticblood disorder

Hereditary ,chronichaemolytic anaemia

affects principally

black populations

mainly affects people from theMediterranean

Abnormal hemoglobin calledhemoglobin S. A genetic errormakes the hemoglobin moleculesstick together in long, rigid rodsafter they release oxygen. Theserods cause the red blood cells tobecome hard and sickle-shaped,unable to squeeze through tinyblood vessels causing a blockagethat deprives the body's cells and

tissues of blood and oxygen.

The rate of production of certainhemoglobins is decreased leading toan imbalance of globin chainsavailable for hemoglobin dimerconstruction.

This results in the formation ofabnormal amounts of structurallynormal (normal amino acidsequence) hemoglobins.

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Sickle cell anaemia Thalassaemia (Cooley'sanaemia

Evidence in the skull vault of:

- Thickening of the frontal and parietalbones

-Widening of the diploic space

-Thinning of the inner and outer tables

-Generalized osteoporosis

-The hair-an-end appearance

Evidence in the skull vault of:

- Widening of the diploic space

-Thinning of the inner and outer tables

-Remodeling of the trabeculae to givesparse lines which may

radiate outwards from the inner tableproducing the hair-on-end

Evidence in the jaws of:

A generalized coarse trabecular pattern

-Fewer trabeculae are evident

- Enlargement of the maxillae, with

protrusion and separation ofthe upper anterior teeth

Osteosclerotic areas resulting from theinfarcts

- Usually normal teethwith normal laminadura.

Evidence in the jaws of :

-Generalized coarse trabecular pattern

-Thinning of all cortical structures

- Expansion, which lead to

encroachment on, and subsequentobliteration of the maxillary antra

-No evidence of bone infarcts.

- Apparent spike-shaped or shortenedtooth roots

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Sickle cell anaemia


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Thalassaemia


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Systemic Diseases Manifested in the Jaw.ppsx

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