3. Cemento‐Osseous Dysplasia
A spectrum of dysmorphic bone and cementum
Types.
• Periapical cemento‐osseous dysplasia
• Florid cemento‐osseous dysplasia
• Focal cemento‐osseous dysplasia
4. PATHOGENESIS
Mesenchymal stem cells lost their ability to maintain their structural morphology
and therefore, produce what is termed Dysplastic CEMENTO-OSSEOUS TISSUE
5. Periapical Cemento‐Osseous Dysplasia
• Asymptomatic set of lesions that form around the apex of mostly mandibular
vital anterior teeth
• Radiolucent to mixed radiolucent‐radiopaque to completely radiopaque
without a change in the root structure or tooth vitality
• Black women of AFRICAN heritage around the age of 40 years
• Usually an incidental radiographic finding because these lesions do not induce
tooth mobility or bony expansion.
6.
7. FLORID Cemento‐Osseous Dysplasia
• Extended form of periapical cemento‐osseous dysplasia
• Radiolucent‐radiopaque periapical and interradicular lesions involving the
mandible bilaterally and the maxilla.
• Asymptomatic dysmorphic bone‐cementum complexes.
• About 10% become exposed to the oral flora because of tooth removal,
periodontal disease, or pulpal disease and become painful because of
secondary infection.
8. Florid cemento‐osseous dysplasia will have radiopacities in several quadrants, which
will obliterate tooth root outlines. Involvement is limited to the tooth‐bearing
alveolar bone and spares the rami and basilar bone.
10. DIFFERENTIAL DIAGNOSIS
• Diffusely positioned, radiopaque masses in the jaws may suggest a syste
mic etiology, most importantly Paget disease or the multiple endosteomas
in Gardner syndrome.
• If it cannot be distinguished from Paget disease radiographically, an
alkaline phosphatase determination is needed.
• If Gardner syndrome is a strong consideration, a skull series and other
radiographs to search for osteomas elsewhere, as well as a colonoscopy,
are recommended.
11. Focal Cemento‐Osseous Dysplasia
• An incomplete form of florid cemento‐osseous dysplasia that is
much less common.
• Develops in a single focus in the alveolar bone .
12. Focal cemento‐osseous dysplasia will present as a single area or as two close‐
together areas representing a less severe form of florid cemento‐osseous dysplasia but making it less
distinguishable from other radiopaque lesions.
13. HISTOPATHOLOGY
• Initially - vascular fibrous tissue with no capsule.
• Over time, an increasing quantity of mineralized tissue develops, which may
take the form of rounded, cementum‐like material and/or osseous trabeculae.
• Eventually, there is coalescence of this material with formation of a sclerotic,
avascular, and acellular mass.
14. A fibrous stroma within which rounded and trabecular cemento‐osseous tissue is randomly arranged.
15. The Cemento-osseous
Dysplasias.
(a) Early stage lesion
with hemorrhagic foci,
(b). Early region with
fibro-
osseous pattern,
(c). Mid stage lesion
with progressively more
trabeculae,
(d). Late stage lesion
with sclerotic bone.
(e) Late stage lesion
with ‘‘ginger root’’
curvilinear confluent
trabeculae
18. FCOD OF
An irregular mixed radiolucent-opaque
pattern (69%) with slightly more than half
of cases showing well-defined borders.
More than half of OF present as a pure
radiolucency with significantly larger size
and typically cause jaw expansion clinically.
FCOD shows a close association with
tooth apices (70.6%) or with previous
extraction sites (21%).
Majority of OF (86%) shows no
relationship with either.
Benign nonneoplastic process OF is a true neoplasm
19. DIAGNOSIS AND TREATMENT
• Biopsy is not usually required. The clinical history, age, race, sex, and
radiographic findings are sufficient to diagnose most cases.
• Because this phenomenon is not - progressive, symptomatic, or
particularly damaging, no treatment is required.
20. • If tooth removals, the roots are ankylosed to the bone‐cementum complex
which has poor cellularity and vascularity;
wound that remains exposed and does not heal--
secondarily infected wound and the onset of pain and drainage
21. Surgery for florid cemento‐osseous dysplasia will identify avascular
discolored bone with some granulation tissue. The diseased bone is usually separated from normal bone
by granulation tissue. When it is not, it is more difficult to remove.
24. Hyperparathyroidism
• Caused by hypersecretion of parathyroid hormone (PTH)
• Hyperplastic glands- Primary/Secondary.
• Hypercalcemia ≥10.5 mg/dl [2.6 mmol/L.
• 5% of cases are recognized by the presence of an osteolytic defect with giant cells, -
Brown tumor.
• Some cases are suspected by the presence of renal stones (nephrocalcinosis).
25. • women
• Older than 50 years.
• Most gland hyperplasias are of unknown cause, but some are related to the multiple
endocrine neoplasia syndrome of familial inheritance types i and iia (MEN I AND MEN
IIA).
• Because most cases are due to an idiopathic hyperplasia of each gland, a neck mass is
usually not palpable.
• Most cases are asymptomatic. However, as serum calcium levels increase, symptoms
may occur that are related to the hypercalcemia per se or to the disease's effects on bone
and on the urinary tract.
26.
27. Bone‐Related Signs and Symptoms
• Bone pain is the main symptom and occurs primarily in the vertebrae, tibias, and
joints
• Long‐standing disease can produce kyphosis and multiple small vertebral fractures
that can lead to loss of height.
• Radiolucencies (brown tumors) may develop in bones, commonly in the jaws
or a diffuse demineralization.
28. • Both entities evidence a fibrovascular stroma replacing mineralized bone. These are
as appear as a friable, red‐brown mass, hence the term BROWN TUMORS.
This mandibular radiolucency was asymptomatic and
caused a slight expansion. It was thought to be anothe
r entity but was confirmed to be a brown tumor by
biopsy and a serum calcium determination, which id
entified a 14.1 mg/dL value
This known brown tumor of hyperparathyroidism
was identical to the more common giant cell
tumor. It was friable, hemorrhagic, and reddish
brown.
34. HISTOPATHOLOGY
• Identical to that of the central giant cell tumor.
• A proliferation of spindle cells.
• Extravasated blood .
• Variably sized multinucleated giant cells is seen.
• These are osteoclasts.
36. TREATMENT
• Medical treatment for primary hyperparathyroidism is indicated only in those in whom
surgery is contraindicated and in those with mild hypercalcemia (< 11 mg/Dl)
[2.75 mmol/L], albumin corrected) who show no evidence of organ dysfunction.
• Most patients with primary hyperparathyroidism require surgery.
• Surgery involves removal of at least three of the four glands and, in some cases, a sub
total resection .
37. TREATMENT
• Treatment consists of increased fluids, exercise, avoidance of prolonged inactivity, and
avoidance of thiazide diuretics, because these drugs decrease calcium excretion and
raise serum calcium levels.
• For postmenopausal patients, estrogen hormone therapy also may be considered.
39. OSSIFYING FIBROMA (CEMENTIFYING
FIBROMA; CEMENTO-OSSIFYING FIBROMA)
• Ossifying fibroma is a true neoplasm with a significant growth potential.
• True ossifying fibromas are relatively rare
• Variable mixture of bony trabeculae, cementum-like spherules, or both.
• All of these variations will be combined under the term, ossifying fibroma.
40. Clinical features
• 3-4 decades of life.
• Female
• Mandible > maxilla
• Mandibular premolar and molar.
• Painless swelling of the involved bone
• May cause obvious facial asymmetry
• Rarely pain and paresthesia
41. Radiographic features
• Well defined and unilocular
• Depending on the amount of calcified material, may appears with varying
degrees of radiopacity.
• Large ossifying fibromas of the mandible often demonstrate a characteristic
downward bowing of the inferior cortex of the mandible.
46. Treatment and Prognosis
• Circumscribed nature of the ossifying fibroma generally permits
enucleation of the turnor with relative ease
• Prognosis is very good.
• Recurrence after removal is rarely encountered.
• No evidence that ossifying fibromas ever undergo malignant change.
48. JUVENILE OSSIFYING FIBROMA
(JUVENILE ACTIVE OSSIFYING FIBROMA;
JUVENILE AGGRESSIVE OSSIFYING FIBROMA
• Distinguished from the larger group of ossifying fibromas on the basis of the age
of the patients, most common sites of involvement, and clinical behavior.
• Two patterns: (1) Trabecular,
(2) Psammomatoid.
49. Clinical and Radiographic Features
• No significant sexual predilection
• Well-circumscribed. And lack continuity with the adjacent normal bone.
• Trabecular form is diagnosed initially in younger patients; mean age = 11
years.
• Psammomatoid variant approaches 22 years.
• Reveal a maxillary predominance.
• Cortical expansion facial enlargement
50. • Trabecular variant shows irregular strands of highly cellular osteoid and
irregular osteocytes
51. • Psammomatoid pattern forms
concentric lamellated and spherical
ossicles that vary in shape and typically
have basophilic centers with
peripheral eosinophilic osteoid rims
52. Treatment and Prognosis
• Many tumors demonstrate slow but progressive growth, some juvenile ossifying
fibromas demonstrate rapid enlargement.
• For smaller lesions, complete local excision or thorough curettage appears adequate.
• For some rapidly growing lesions, wider resection may be required.
• Recurrence rates of 30% to 58% have been reported for juvenile ossifying fibromas.
• Malignant transformation has not been documented .
In fact, cemental and osseous are often used interchangeably because both cementum and bone originate from mesenchymal stem cells
However, these cells are not neoplastic, nor are they premalignant. Instead, these cells produce morphologically imperfect bone or cementum; therefore, the term dysmorphic bone is preferred.
The natural radiographic course of periapical cemento‐osseous dysplasia is
illustrated in this series of periapical radiographs: (a) beginning radiolucencies; (b and c) beginning and
more mature radiopacities creating a more dense, irregular, mixed radiolucent‐radiopaque
appearance; (d and e) mature radiopacities creating a pure, well‐outlined radiopaque appearance.
This sequence was recorded over a period of 18 years.
(Photomicrographs from periapical cemento‐osseous dysplasia showing the changes that occur over time. This histology is shared by all types of cemento‐osseous dysplasia.)
(A) Intraoral periapical radiograph, (B) shows mixed lesion, (C) shows opaque lesion
Situated unusually at the periapex of a pulpless tooth in which usually the root canals have been successfully filled. It represents a previous periapical granuloma, cyst or abscess whose healing has terminated in the formation of dense scar tissue.11 When the periapical scar is associated with an asymptomatic root canal filled tooth, it requires no treatment.
On gross examination, the lesion is
typically comprised of multiple tan and brown tissue
aggregates that appear crumbly
Wiki ---------
The plasma level of calcium is closely regulated with a normal total calcium of 2.2-2.6 mmol/L (9-10.5 mg/dL) and a normal ionized calcium of 1.1-1.4 mmol/L (4.5-5.6 mg/dL). The amount of total calcium varies with the level of serum albumin, a protein to which calcium is bound. The BIOLOGIC EFFECT OF CALCIUM IS DETERMINED BY THE AMOUNT OF IONIZED CALCIUM, rather than the total calcium. Ionized calcium does not vary with the albumin level, and therefore it is useful to measure the ionized calcium level when the serum albumin is not within normal ranges, or when a calcium disorder is suspected despite a normal total calcium level.
Corrected calcium level[edit]
One can derive a corrected calcium (also known as adjusted calcium) level, to allow for the change in total calcium due to the change in albumin-bound calcium. This gives an estimate of what the total calcium level would be if the albumin were a specified normal value. Exact formulae used to derive corrected calcium may depend on the analytical methods used for calcium and albumin. However the traditional method of calculating it is shown below.
Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 - serum albumin [g/dL]), where 4.0 represents the average albumin level in g/dL.in other words, each 1 g/dL decrease of albumin will decrease 0.8 mg/dL in measured serum Ca and thus 0.8 must be added to the measured Calcium to get a corrected Calcium value.
Or: Corrected calcium (mmol/L) = measured total Ca (mmol/L) + 0.02 (40 - serum albumin [g/L]), where 40 represents the average albumin level in g/Lin other words, each 1 g/L decrease of albumin, will decrease 0.02 mmol/L in measured serum Ca and thus 0.02 must be added to the measured value to take this into account and get a corrected calcium.
When there is hypoalbuminemia (a lower than normal albumin), the corrected calcium level is higher than the total calcium.
Most gland hyperplasias are of unknown cause, but some are related to the multiple endocrine neoplasia syndrome of familial inheritance types i and iia (MEN I AND MEN IIA).
lesion derives i ts name from the
color of the t issue specimen. which is usuall y a dark
reddish-brown because of the abundant hemorrhage
and hemosiderin deposit ion within the tumor. These
lesions appear radiographically as well-demarcated
unilocular or multilocular radiolucencies
osteitis fibrosa cystica, a condition that
deve lops from the central degenerat ion and fibros is of
longstanding brown tumors.
An IOPA radiograph showing complete loss of LD in a PHPT patient
An OPG showing reduced cortical width of the mandible and a ground glass appearance in a PHPT patient
PHOSPHATE--its excretion is enhanced by PTH, which prevents phosphate reabsorption. Therefore, serum phosphate concentrations are the inverse of serum calcium concentrations in each type of hyperparathyroidism. In primary hyperparathyroidism, the excess PTH produces a
hypophosphatemia by increasing renal loss. In secondary hyperparathyroidism, urinary phosphate loss
is reduced by the lack of glomerular filtration of phosphate and the ineffective response to PTH,
resulting in hyperphosphatemia.
Bone‐related ALKALINE PHOSPHATASE is an enzyme secreted by osteoblasts that hydrolyzes organic
phosphates for bone mineralization. ELEVATIONS ARE A ROUGH INDEX OF NEW BONE FORMATION. In all of the
hyperparathyroidisms, alkaline phosphatase levels are normal because in most cases the serum
hyper‐ and hypocalcemias and the hyper‐ and hypophosphatemias are unrelated to new bone
formation.
well-circumscribedsolid tumormass.
Trabeculae of bone and droplets of cement um-like material can be
s een formingwithin a background of cellular fibrousconnective
tissue.
The word "psammoma" is derived from a greek word "psammos" meaning "sand."
Trabeculae of cellular
woven bone are present in a cellular fibrous stroma.
Cellular fibrous con-
nective tissue containing spherical ossicles with basophilic centers
and peripheral eosinophilic rims.