peripheral giant cell granuloma (giant cell epulis

GIANT CELLS LESIONS OF THE JAW

DEPARTMENT OF ORAL MEDICINE

Classification of giant cells lesions of jaw

I. Reactive disorders of bone (a) Central giant cell granuloma (b) Primary hyperparathyroidism

II. Tumors of the bone Giant cell tumor (osteoclastoma) Idiopathic histiocytosis (Langerhans cell diseases) -Letterer Siwe disease -Hand-Schuller Christian syndrome - Eosinophilic granuloma

III. Connective Tissues Hyperplasia Peripheral giant cell granuloma (Giant

cell epulis)

IV. Non-epithelialized primary bone cyst

Aneurysmal bone cyst Solitary bone cyst (simple bone cyst,

traumatic bone cyst)

V. Fibroosseous lesions Fibrous dysplasia Cherubism

Giant Cells Ultrastructurally → Derived from mononuclear phagocyte system (macrophages)

Show features of osteoclasts Immunohistochemically →

macrophages and giant cells have similar antigenic marker such as muramidase α-1 antichymotrysin.  

Giant cells

Peripheral Giant Cell Granuloma (Giant Cell Epulis)

Dept: of Oral medicine

UDM ( Mdy:)

One of the reparative hyperplasias commonly seen in oral mucous membrane representing an exuberant reparative response.

It does not represent a true neoplasm but is a reactive lesion caused by local irritation or trauma.

Distinguishing feature of this lesion is appearance of multinucleated giant cells

CLINICAL AND RADIOGRAPHIC FEATURES

Occurs exclusively on the gingiva usually in the area between first permanent molars and incisors.

Red or Reddish-Blue nodular mass (sessile or pedunculated)

Clinical appearance is similar to the pyogenic granuloma of the gingiva (PGG → more bluish-purple compared with bright red of a typical pyogenic granuloma).

Peak prevalence → 5th and 6th decades of life.

♀ > ♂ (60%); Either anterior or posterior regions of gingiva or alveolar mucosa;

Mandible > maxilla If arising from periodontal ligament or

periosteum → Bone resorption (+) X-ray → Cup-shape radiolucency (cupping

resorption of underlying alveolar bone)

Lack of involvement of bone

cuff-shaped radiolucency at the entrance to the alveolus of clinically vital tooth 12.

Cup-shaped osseous defect at 12 teeth

HISTOLOGICAL FEATURES

Basically → Hyperplastic granulation tissues (+)

Proliferation of multinucleated giant cells within a background of plump ovoid and spindle-shaped mesenchymal cells

Acute or chronic inflammatory cell (+)

Lack of mature collagen, abandance of cells

Peripheral giant cell granuloma arising interdentally

Multinucleated giant cells in peripheral giant cells granuloma

TREATMENT AND PROGNOSIS

Local surgical excision down to the underlying bone

The adjacent teeth should be carefully scaled to remove any source of irritation and minimize the risk of recurrence.

D/D OF PGG

Pyogenic granuloma (PGG → more likely to cause bone resorption than pyogenic granuloma)

Central giant cell granuloma (Which is derived from medullary tissues of mandible and maxilla)

(Clinical features adequately separate these microscopically identical lesions; PGG and CGG)

CENTRAL GIANT CELL GRANULOMA

(GIANT CELL TUMOR)

Benign process exclusively occurs within jaw bones

AETIOLOGY AND PATHOGENESIS

Three possible causes:

1. Reparative response to intrabony haemorrhage and inflammation

2. A lesion considered to be a true neoplasm

3. Developmental anormaly closely related to A.B.C (Aneurysmal Bone Cyst)

CLINICAL AND RADIOGRAPHIC FEATURES

> 60% of cases → occur before age 30 Less frequent than PGG ♀ > ♂(2:1); mandible > maxilla (70%);

more common in anterior portions of the jaws

Mandibular lesions frequently cross the midline

Most of the cases → Asymptomatic Minority of the cases → Associated with

pain, paraesthesia or perforation of cortical plate

Based on clinical and radiographic features, CGG can be divided into two categories: (A) Non Aggressive lesions No symptoms Slow growth No cortical perforation (B) Aggressive lesions

Pain Rapid growth Cortical perforation and root resorption

(+) Marked tendency to recur after treatment.

X-ray = unilocular (or) multilocular radiolucency with well-demarcated presenting scalloping border

Radiographic finding - not diagnostic (small unilocular → Periapical granuloma

(or) cysts multilocular → Amelobastomas)

Multilocular radiolucency with expansion of jaw bone in central giant cells granuloma

Expansion of occlusal projection and multilocular radiolucency across the midline in CGCG

RADIOLUCENCY In midline of mandible,CGCG

Unilocular radiolucency with well defined margin in premolar area ,CGCG

CGCG

HISTOLOGICAL FEATURES Many multinucleated giant cells in

background of ovoid to spindle-shaped mesenchymal cells

Giant cells Small and irregular in

shape

Large, round containing

20 (or) more nuclei Connective tissue stroma Loosely

arranged

Cellular

TREATMENT AND PROGNOSIS

Surgical management with aggressive curettage of tumor mass followed by removal of peripheral bone margin → Good prognosis and low recurrence rate

15 - 20% recurrence rate (+)

Patients with aggressive tumors, three alternative to surgery

(1) Corticosteroids

(2) Calcitonin

(3) Interferon α 2A

(Weekly injection directly into the tumor with triamcinolone acetonide x 6 weeks → success + +)

cases resistant to intralesional steroids→Salmon calcitonin (Systemic administration)

Intradermal Injection of calcitonin _12 months

These alternatives can be used for large lesions if treated surgically would result in significant deformity

D/D of CGG

Due to multilocular radiolucency,

1. Ameloblastoma

2. Odontogenic myxoma

3. Odontogenic keratocyst

4. ABC

Histological features of CGG is identical to brown tumor of hyperparathyroidism but no changes in blood chemistry in CGG

In case of hyperthyroidism

- ↑ Serum Ca + +

- ↑ Serum alkaline phosphatase

- ↓ Serum phosphorus value