Textbook of Oral Pathology Shafers

Textbook of General Pathology

Harsh Mohan
Harrisons Textbook of Internal
Medicine
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Introduction
Types of Rickets
Clinical Features
Radiographic Features
Oral manifestations
Histopathology
Treatment and Prognosis
Rickets : It is a disorder primarily canned by lack of
vitamin D or abnormal metabolism.
The term Rickets is derieved from the English word
Wricken which mean to bend.
It is found in children prior to closure of growth plates.


1. Vitamin - D deficient rickets.
2. Vitamin D resistant rickets.
3. Renal rickets.
4. Osteomalasia [adult rickets].


Synonyms : Familial hypophosphatemia, phosphate
diabetes, refractory rickets.

Definition : Vitamin D resistant rickets is an X-linked
dominant inherited kidney disorder characterized by
hypophosphatemia and hyperphosphaturia.
a) Hypophosphatemia and hyperphosphaturia
associated with decreased renal tubular reabsorption
of inorganic phosphates.
b) Familial occurrence, being inherited as an X-linked
dominant trait.
c) Does not respond to the usual doses of vitamin D.
d) Normocalcemia with high noraml parathyroid
hormone levels.
e) Diminished intestinal calcium and phosphate
absorption.

f) Decreased growth with short stature.
g) Normal vitamin D metabolism.
h) The absence of other related abnormalities.


Since these characteristic features of rickets do not
respond to the therapeutic doses of vitamin D,
hence it is known as vitamin D resistant rickets.

Occurs in childhood
Male > Female.
Widened joint spaces and flaring at knees
Bowing of long bones When child begins to walk
In adults because of rickets in childhood leads to
more serious disturbance such as,
1. Bowing of legs.
2. Shortening of stature.
3. Continuing osteomalacia.
4. Presence of pseudofracture.




The history or X-ray examination reveals
abnormalities such as
1. Skull deformities.
2. Retardation of eruption of teeth.
3. Sitting deformities of legs.
1. There is histologic evidence of widespread
formation of globular, hypocalcified dentine with
clefts and tubular defects occuring in the region of
pulp horns.
2. Pulp horns are elongated and extend high, reaching
nearly to the DEJ.
3. Large pulp chambers.
4. Because of these defects there is commonly
invasion of pulp by micro organisms which leads to
presence of multiple dental abscess.
5. Periapical involvement of grossly normal appealing deciduous
or permanent teeth.
6. Followed by development of multiple fistulas.
7. Abnormal cementum
8. Lamina dura absent or poorly defined on xray
9. Abnormal alveolar bone pattern.
10. Width of predentin is increased.
11. Recently formed dentin is incompletely calcified.
12. Taurodontism was found in permanent molars as a feature of
the condition in the more severly affected male subjects.

Fistula
Dental
abscess
Lamina dura absent or poorly defined.
Abnormal cementum.
Larger pulp chamber.
Abnormal alveolar pattern.

Alternation found primarily in the cartilage plate and
shaft of long bone.
Failure of bone salts to deposit in the cartilage matrix
between the rows of hypertrophic cells.
Histologic picture characterized by a broad zone
between the multiplying cartilage cells and the shaft,
hence called Rachitic Metaphysis.
Broad zone is composed of tongues of cartilage
which extends towards the shaft and separates from
one another by collection of capillaries.

Broad zone contains trabeculae made of uncalcified cartilage
matrix upon which osteoid bone has deposited.
Osteoid is found deposited on pre existing bony trabeculae
because osteoblastic activity is not affected, but calcification
is interfered so the osteoid does not calcified and not
remodeled.

Biochemical findings :

Serum calcium : Normal
Serum PTH : Normal or slightly increased
Calcitriol level : Low
Serum 25 [OH] cholecalciferol : Normal
Urinary loss of phosphate : High

Highly individualized.
Massive dose of vitamin D is given = Risk of
hypervitaminosis.
Success was reported with 25 [OH] cholecalciferol in lower
dosage
i.e., 10,000 25,000 IU/day.
Healing initiated by methods like
1. Immobilization + administration of large amount
of phosphate.
2. Low dosage of vitamin D i.e., 15,000 50,000
IU/day + supplemental oral phosphate.
Endodontic treatment to the non vital teeth.


Synonym: Renal osteodystrophy.

Definition : Renal rickets is a painful crippling bone disease
commonly found in patient with chronic renal failure where
there is a inability of diseased kidney to synthesize 1- alpha
hydroxylase enzyme and convert 25 [OH] cholecalciferol to
active form of vitamin D.

Failure of kidney

No activation of vitamin D

Calcium absorption in intestine is impaired

Fecal calcium excretion [negative calcium balance]

Increased in serum phosphate level[phosphatemia]
Secondary reduction in serum calcium level to maintain stable
calcium/phosphate solubility products.


Compensatory increase in PTH production
[secondary hyperparathyrodism].


Superimposed osteitis fibrosis cystica.
Serious in children, in which legs bend inward
towards each other or outwards away from each
other.
In adult bone changes begins years before symptoms
appear with kidney disease, so called silent
crippler.
Older patient and women in menopausal age are at
greater risk.
Increased risk for bone fracture.
If renal failure begins at young age enamel
hypoplasia occur on developing teeth.
Tooth mobility.
Malocclusion.
Development of pulp stone.
Radiographic alteration of jaw bones are common
in patient undergoing dialysis.
Bone resorption results in
1. Loss of lamina dura
2. Thinning of cortical plate
3. Blurring of anatomic landmarks like mental
foramen, inferior alveolar canal and floor of
maxillary sinus.
Dihydrotachysterol [vitamin D analogue]
1-alpha hydroxycholecalciferol.
Renal transplantation.
Dietry changes should be done like milk, cheese,
dried beans, peas, nuts should be consumed.
Should decrease the consumption of drinks such as
cocoa, beer.
Prognosis of bone disease is difficult because of
inability to cure underlying renal disease.