Cysts of the jaws

Classification of cyst of the jaws

Developmental cyst

odontogenic

· Gingival cysts of infants (epstain pearls)

· Odontogenic kerato cyst(primodial cyst)

· Orthokeratinized odontogenic cyst

· Dentigerous (follicular cyst)

· Eruption cyst

· Lateral periodontal cyst

· Gingival cyst of adults

· Glandular odontogenic;sialoodontogenic cyst

Non-odontogenic cyst

· Nasopalatine duct cyst

· Nasolabial cyst

Inflammatory odontogenic cyst

Radicular

· Residual

· Lateral

Paradental

Key features of jaw cysts

· Form sharply defined radiolucencies with smooth borders.

· Fluid may be aspirated and thin walled cysts may be trans illuminated.

· Grow slowly,displacing rather than resorbing teeth.

· Symptoms unless infected and are frequently chance radiographic findings.

· Rarely large enough to cause pathological fracture.

· Form compressible and fluctuent swellings if extending in to soft tissues.

· Appear bluish when close to the mucosal surface

Major factors in the pathogenisis of the cyst formation

· proliferation of epithelial lining and fibrous capsule

· hydrostatic pressure of cystic fluid

· resorption of surrounding bone.

Teeth Discolouration (Teeth staining) and Treatments

Teeth Discolouration (Teeth staining) and Treatments

Dentition is considered to be a major part of aesthetics where people spend huge amount of money on maintaining it nicely. When we consider the conditions affecting teeth, discolouration is one of the main conditions people worry about. Aetiology of teeth discolouration is multifactorial. Coronal parts of the crown of the teeth are composed of Enamel, Dentine and Pulp. Structural alteration in any of these components would cause teeth to be discoloured.

Aetiology of teeth discolouration

Aetiology of teeth discolouration is multifactorial. Classification of teeth discolouration is described below.

In the previous classifications teeth discolouration is classified according to the location of discolouration, which may be either intrinsic or extrinsic.

Intrinsic discolouration

Intrinsic discolouration occurs due to a change in structural composition or thickness of the dental hard tissues. Several systemic diseases and metabolic disorders are known to affect the developing dentition and cause discolouration. In addition to that trauma is considered to be a local cause of intrinsic discolouration.

• Alkaptonuria
• Congenital erythropoietic porphyria
• Congenital hyperbilirubinemia
• Amelogenesis imperfecta
• Dentinogenesis imperfecta
• Tetracycline staining
• Fluorosis
• Enamel hypoplasia
• Pulpal haemorrhagic products
• Root resorption
• Ageing

Extrinsic discolouration

Extrinsic discolouration is outside the tooth substance and lies on the tooth surface or in the acquired pellicle.

This stains may be

Metallic or non-metallic

Internalized discolouration

Internalized discolouration is incorporation of extrinsic stains in to tooth structure after tooth development.

Roots by which pigments may become internalised are

Developmental defects

Acquired defect eg: tooth wear and gingival recession, dental caries, restorative material

Commonest causes of dental discolouration in modern days

• Foods and drinks: coffee, tea, cola, wines, apples, potatoes
• Tobacco use: Smoking or chewing tobacco can stain the teeth
• Diseases: Amelogenesis imperfecta, Dentinogenesis imperfecta
• Pregnancy
• Head and neck radiation and chemotherapy
• Medications: eg-tetracycline, certain anti histamines
• Dental materials
• Advancing the age
• Genetics
• Environment
• Trauma

Treatment for dental discoluration

Proper tooth brushing and flossing

Teeth whitening agents

Bondings-Tooth coloured resin material is applied and cured with light

Veneers-Custom made shells of the teeth are fixed on to the tooth surface. There are two typs of veneers commonly used these days. They are porcelain and resin veneers.

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Mouth Ulcers

http://dentistryandmedicine.blogspot.com/2010/12/causes-for-oral-ulceration.html

Causes for Oral Ulceration

Oral ulcers

Oral ulceration is probably the commonest oral mucosal condition encountered by a dentist or doctor. Oral ulcers are usually accompanied by pain except when an early malignant lesion presents as painless ulcers. Oral ulceration is “discontinuation of oral epithelium”.
Oral ulcers could occur due to various causes

• Trauma-mechanical, chemical, thermal, radiation
• Aphthous ulceration-major, minor, herpetiform
• Infections-viral, bacterial, protozoal
• Haematological-Haematinic deficiency, neutropenia, Leukaemia
• Gastrointestinal-coeliac disease, crohn’s disease, ulcerative colitis
• Mucocutaneous-Oral lichen planus, pemphigus, pemphigoid, Erythema Multiforme
• Drugs

Oral Carcinosarcoma

Carcinosarcoma Definition

A malignant neoplasm that contains elements of carcinoma (cancer of epithelial tissue, which is skin and tissue that lines or covers the internal organs) and sarcoma (cancer of connective tissue, such as bone, cartilage, and fat) so extensively intermixed as to indicate neoplasia of epithelial and mesenchymal tissue.

Source: National Institute of Health-USA

Synonyms

• Carcinosarcoma(Minkler et.al. 1970)
• Spindle-cell carcinoma or Pleomorphic Carcinoma(Ellis & Corio 1980,Zarbo et.al. 1986,Ellis et.al. 1987)
• Spindle-cell SCC
• Pseudosarcoma(Lane 1957)
• True malignant mixed tumour
• Sarcomatoid carcinoma

Epidemiology

Extremely RARE.

Head-and-neck sites ; in descending Frequency

Larynx

Oral cavity

Hypopharynx and pyriform sinus

Sinonasal tract

Oropharynx

Carcinosarcoma (CS) is sometimes found in other parts of the body.

Incidence is more common in the upper body, particularly the lungs

In oral cavity carcinosarcoma can arise from either salivary glands or oral mucosa.

Aetiology

Idiopathic

Radiation /trauma has been emphasized by some authors (Green & Bernier 1959)

Accumulation of genetic mutations could be a factor.

Clinical Features

Symptoms are often present for a short duration

Nearly all cases are described or received as;

• Polypoid masses .
• Mean size of about 2.0cm
• Frequently ulcerated.
• With a covering of fibrinoid necrosis.
• Firm and fibrous cut surface.
• (Similar to conventional SCC, most tumours are T1 lesions at presentation.)

These carcinosarcomas occur most frequently on the lower lip,tongue and alvelolar ridge in either polypoid,exophytic or endophytic configurations.

Surface ulceration is common with these tumors. As with any ulcerated lesion, these are likely to be infected and therefore may exude pus or contain abscess formation.

Cervical lymphadenopathy is infrequent,distant metastasis may/not present.

Investigations

MRI

CT

Scintigraphy

Histopathological investigations;

- Incisional biopsy

- Excisional biopsy

- Immunohistopathological investigations.

Ultra sound scanning to detect lymph node involvement.

Chest X-ray & Gastroendoscopy to detect distant metastases.

HISTOLOGY

Carcinosarcoma composed of heterologous malignant epithelial & stromal components which both fulfill histological criteria of malignancy.

Usually Sarcomatous component is predominent.

Biphasic presentation

Ulcerated

Carcinomatous component is either blended or in transition with sarcomatous component.

Hypercellularity

Variable patterns of spindle-cell growth in sarcomatous component

Pleomorphism

Increased mitotic figures

Carcinomatous component is usually

• Undifferentiated SCC
• Squamous cell carcinoma
• Poorly differentiated adenocarcinoma
• It may also include
• Adenoid cystic carcinoma
• Epithelial myoepithelial carcinoma
• Salivary duct carcinoma.

The sarcomatous component is usually,

Undifferentiated spindle cell sarcoma

Other reported sarcomatous elements include

• Fibrosarcoma
• Osteosarcoma
• Leiomyosarcoma
• Liposarcoma
• Follicular dendritic cell sarcoma
• Undifferentiated sarcoma
• Myxoid sarcomas
• Rhabdomyosarcoma
• Chondrosarcoma

Areas of squamous differentiation are most consistently identified at the base of the polypoid lesion, at the advancing margins, or within invaginations at the surface where the epithelium is not ulcerated or denuded.(Condition is same in our patient)

CS will often present with little invasion into the underlying stroma, as it is polypoid.

Extensive infiltration and tissue destruction are common, as is perineural invasion and angioinvasion. Lymphatic spread is less common.

Metastases to other sites or lymph nodes may show the carcinomatous or the sarcomatous components alone, or they may be mixed.

So its extremely difficult in making the correct diagnosis of this tumor from a small biopsy specimen.

It is well illustrated by varies diagnoses based on biopsy specimens.

Immunohistochemistry

Immunohistochemical markers are used in aid of diagnosis.

Eg; -Cytokeratin

- Vimentin

- S-100

- Actin

Cytokeratins are proteins of keratin-containing intermediate filaments found in the intracytoplasmic cytoskeleton of epithelial tissue.there fore carcinomatous componentwhich is derived from epithelial tissue is strongly positive for cytokeratin

Vimentin is a member of the intermediate filament family of proteins that is especially found in connective tissue. This filament is used as a marker for mesodermally derived tissues, and as such can be used as an immunohistochemical marker for sarcomas.

Immunohistochemistry for smooth muscle actin & vimentin reveals positivity in spindle cell component while the squamous cell component shows cytokeratin positivity.

S-100 is negative.

Our patient’s immunohistochemical profile

HISTOPATHOGENISIS

Two antithetical hypotheses have been advanced to explain the histogenesis of carcinosarcomas:

Multiclonal origin/ convergence hypothesis-arising from two or more stem cells

Monoclonal origin/ Divergence hypothesis-from a single totipotential stem cell that differentiates in separate epithelial and mesenchymal directions.

Recent immunohistochemical and chromosomal analyses appear to have settled this argument in favour of the monoclonal hypothesis.

But some of the cases showed a sharp demarcation between the carcinomatous & sarcomatous elements without transition zone & different immunohistochemical staining pattern of the two components for epithelial & mesenchymal markers which suggests a different cell origin for each tumor cell types.

However possibility remains that the demarcation may not signify a different origin, since carcinoma components are demarcated in some sarcomatoid carcinomas in which the sarcomatous component derives from metaplasia of the epithelial cells.

Treatment modalities for sarcomatoid carcinoma.

The primary treatment modality for sarcomatoid carcinoma should be the same as for squamous cell carcinoma which consists of;

SURGICAL EXCISION of the lesion with an adequate margin.

ADJUVANT IRRADIATION may be beneficial in patients who have positive surgical margin or who have nodal metastasis.

The role of the chemotherapy has not been established, but it may decrease the incidence of recurrence or metastasis of primarily sarcomatous tissue.

Prognosis

Mean survival time of those dead of the disease is

2 years.

No clinical or histomorphological characteristic other than distant metastasis was found to be a reliable prognostic indicator.

Calcifying Epithelial Odontogenic Tumour (Pindborg's Tumour)

Calcifying Epithelial Odontogenic Tumour (CEOT) is a rare, benign odontogenic neoplasm which accounts for less than 1% of all odontogenic tumours . It was first described by the Dutch pathologist Jens Jorgen Pindborg in 1955. CEOT is also called as “Pindborg’s tumour” which, the term was introduced by Shafer et.al in 1963. It was previously described as an adenoid adamantoblastoma, unusual ameloblastoma and a cystic odontoma. The term ‘Calcifying Epithelial Odontogenic Tumour’ has been generally accepted and adopted by the WHO in 1971,7 J.J. Pindborg and I.R.H. Kramer, Histological typing of odontogenic tumors, jaw cysts and allied lesions, WHO, Geneva (1971). when it was recognized as a distinct entity.

The age range is wide 8-92 years, although it is most commonly seen in the fourth and fifth decade of life. CEOT may occur as intraosseous tumours or extra osseous tumours. The extraosseous variant is diagnosed slightly earlier (mean age 34.4 years) than the intraosseous type (mean age 38.9 years). They appear to be no sex predilection.

Mandible is more commonly affected than maxilla in ratio of 3:1 and it is usually located in the premolar and molar regions. When present in the maxilla, the CEOT is preferentially located in the posterior region. The prevalence in the molar region is three times that in the premolar region. CEOT with extension into the maxillary sinus is uncommon.

94% of the lesions are central and intraosseous and 6% are extraosseous.

Clinically, it presents as a slowly growing expansile jaw lesion, which may be associated with pain, nasal airway, obstruction, epistaxis and headache. Maxillary, tumors may present with facial alteration and proptosis. It may cause tooth tipping, migration, rotation and/or mobility secondary to tooth resorption. CEOT is often concurrent with an unerupted or impacted tooth (52 % of odontogenic tumours) and rarely associated with paresthesia.

An extraosseous variant of CEOT also presents clinically as a nodular mass on gingival mucosa in anterior tooth location, but this is extremely rare and only 10 cases are reported (5%).

CEOT has also been reported as hybrid tumours in combination with adenomatoid odontogenic tumour which has been reported to be frequent in women and present at younger age.

Depending on stages of development, CEOT may present variable radiographic appearances. The lesion usually consists of a radiolucent area, which is well defined. Area is often unilocular when small and larger lesions tend to have multilocular, honeycomb or soap bubble appearance. Multiple radiopacities of varying size may develop within the radiolucent area and occasionally there extensive areas of calcification that cause the lesion to become radiopaque. The mixed radiolucent and radiopaque pattern occurred most often (65%) followed by the completely radiolucent pattern (32%) and least often the totally radiopaque ‘‘wind driven snow’’ pattern (3%). When tumour is associated with impacted tooth, it may appear as pericoronal radiolucency with or without small radiopacities.

The two commonest presentations were found to be pericoronal radiolucency with diffuse radiopacities in a radiolucent area. This makes the clinical diagnosis somewhat difficult due to the similarity with dentigerous cyst. For extraosseous CEOT, bone adjacent to the tumour shows a superficial erosive pattern.

The clinical differences among the CEOT types have been thought to be attributed to their origin. It has been shown that the intraosseous CEOT is derived from the stratum intermedium of the enamel organ. In contrast the extraosseous form arises from the dental lamina rests in gingiva and/or basal cells of gingiva surface epithelium, but today most investigators believe that the tumour cells originate from the stratum intermedium of the normal dental germ. This idea is based on the morphologic similarity of the tumour cells to the normal cells of the stratum intermedium and on the finding of high activity of alkaline phosphatase and adenosine triphosphate at both sites.

When it comes to the hybrid tumour between CEOT and adenomatoid odontogenic tumour (AOT), It had been postulated that the AOT portion arise from all three components of the enamel organ (Preameloblast, Stellate reticulum, Stratum intermedium).

According to the literature, the characteristic histologic criteria for the diagnosis of CEOT are sheets of large polygonal epithelial cells that have well defined borders and often show prominent intercellular bridges. There is usually pleomorphism of the epithelial cells. Nuclei are often prominent and show considerable variation in size, shape and number. Cellular abnormalities are frequent, whereas mitotic figures are rarely seen, cytoplasm is abundant and eosinophilic. Varying amounts of an extracellular amyloid like material that stains positive with Congo red stain in polarized light is also a typical of these tumours. Concentric calcified masses with a Liesegang’s rings calcification pattern are also pathognomonic for this tumour.

Ai-Ru et.al in 1982 have proposed a sub classification of these features into four main patterns. Although two or more patterns may coexist in the same tumour, a predominance of one type is often seen. Briefly stated those four patterns are,

Pattern 1 - Polyhedral epithelial cell arrangements with deeply eosinophilic cytoplasm and prominent nuclei, cell outlines and intercellular bridges are distinct, frequent cell abnormalities, few or no mitotic figures, and calcifications are present in the fibrous stroma.

Pattern 2- Cribriform appearance of the cell arrangements, intercellular bridges might be discrete; few cell abnormalities, and calcification of the eosinophilic material filling the cribriform spaces with a Liesegang calcification pattern.

Pattern 3- Scattered or dense arrangements of the epithelial cells with varying size and multinucleated giant cells are frequent, mucoid material is present in the stroma.

Pattern 4- Nests and cords of epithelial cells containing either an abundant eosinophilic cytoplasm or a clear vacuolated cytoplasm, variable amounts of stroma containing eosinophilic material, and calcifications.

Histological variants including CEOT with cementum-like components, Clear-cell CEOT (15 cases reported so far), CEOT-containing Langerhans' cells, Combined epithelial odontogenic tumour (CEOT/AOT) and CEOT with myoepithelial cells are discussed in literature.

When clear cells are present with clear cytoplasm, then this variant is referred to as "Clear Cell Variant" or CCEOT. The incidence of the clear cell variant is rare: according to article published in 1994 by Hicks MJ and his colleagues, there were only 9 known cases reported in the literature. However, this indicates that approximately 8% of CEOTs contain clear cells.

Local recurrence rates of 10-15% have been reported and malignant transformation is rare. Clear cell variant of CEOT is reported to be more aggressive and with a higher recurrence rate.

The treatment for CEOT has ranged from simple enucleation or curettage to radical and extensive resection such as hemimandibulectomy or hemimaxillectomy. The choice should be individualized for each lesion because the radiological and histological features may differ from one lesion to another. Since the case reported was of great extension and rapid evolution, the treatment was right mandible segmental resection and titanium plate reconstruction. It could be possible to correlate some characteristics of the gross examination of the surgical resection, like cystic cavity filled with blood, calcified particles, lingual cortex fenestration, multilocular spaces and vascularity, to those found in CT images. The prognosis of the CEOT is good with infrequent recurrence. Malignant behavior is extremely rare. Although it has not been established in the literature, five years should be the absolute minimum follow-up necessary to assess the healing for this type of odontogenic tumor.