Showing posts with label Oral Pathology. Show all posts
Showing posts with label Oral Pathology. Show all posts

Thursday, August 21, 2014

Best of fives for dentistry- Sjögren's syndrome mcq review

                                                           Sjögren's syndrome




What is CREST?
CREST is a form of Systemic Sclerosis (scleroderma) which is characterized by Calcinosis (calcium deposits), usually in the fingers; Raynaud's;loss of muscle control of the Esophagus, which can cause difficulty swallowing; Sclerodactyly, a tapering deformity of the bones of the fingers; and Telangiectasia, small red spots on the skin of the fingers, face, or inside of the mouth. (Also see: What is Scleroderma?, Types of Scleroderma and Systemic Symptoms)
Calcinosis            Raynaud's              Esophagus            Sclerodactyly            Telangiectasia
It takes only two of the five CREST symptoms for a diagnosis of  CREST (either "pure" or "plus") to be made. For example, a patient with Calcinosis and Raynaud's would have CREST (which for precision may also be written as CRest, but it is CREST nonetheless.)

CALCINOSIS
The systemic forms of scleroderma can cause small white calcium lumps to form under the skin on fingers or other areas of the body.
This is called calcinosis . The lumps may break through the skin and leak a chalky white liquid.
These most commonly occur on the hands, or near joints such as elbows or knees, although they may appear anywhere.

Raynaud's
Raynaud's is a vascular disorder commonly found in sclerodema. It is an extreme spasm of blood vessels in response to cold or stress. The fingers and/or toes become white and/or blue, and may become red on re-warming.

sclerodactyly
When the skin on the fingers become tight, stretched, wax-like, and hardened it is called sclerodactyly. Sclerodactyly is commonly associated with atrophy of the underlying soft tissues.

Telangiectasia are dilated superficial blood vessels

Sunday, November 13, 2011

A Note on Bone Swellings in Jaw Bones


Bone Swellings

Bone swellings are lesions that characteristically present as asymptomatic hard lumps, covered by normal epithelium. Developmental disorders, benign and malignant tumors are included in this group of lesions.
  •        Torus mandibularis
  •        Torus palatinus
  •        Multiple exostoses
  •        Osteoma
  •        Osteosarcoma
  •         Chondrosarcoma
  •         Burkitt lymphoma
  •         Multiple myeloma
  •         Paget disease
  •       Odontogenic tumors

Torus Mandibularis
Definition and etiology Torus mandibularis is a developmental malformation of unknown etiology.
Clinical features It presents as an asymptomatic bony swelling, covered by normal mucosa. The lesion displays slow growth during the second and third decades of life. Characteristically, the lesions appear bilaterally on the lingual surface of the mandible, usually in the area adjacent to the bicuspids. The diagnosis is based on clinical criteria.
Torus mandibularis
Treatment Unnecessary unless full denture construction is required.

Torus Palatinus
Torus palatinus at the midline of the hard palate
Definition and etiology Torus palatinus is a developmental malformation of unknown etiology.
Clinical features It presents as a slow-growing, nodular, lobular or spindled, asymptomatic bony swelling covered by normal mucosa. Characteristically, the lesion appears along the midline of the hard palate.It occurs more often in women, and usually appears during the third decade of life. The diagnosis is based on the clinical findings.
Treatment Unnecessary unless full denture construction is required.

Multiple Exostoses
Multiple exostoses may occur on the buccal surface of the maxilla, and rarely on the mandible. Clinically, the lesions appear as multiple asymptomatic bony swellings. The diagnosis is based on the clinical findings.
Multiple exostoses on the maxilla.
Treatment Unnecessary unless full denture preparation is required.

Osteoma
Definition Osteoma is a benign neoplasm that consists of mature compact or cancellous bone.
Etiology Unknown.
Clinical features
It presents as an asymptomatic, slow-growing bony swelling of the jaws. The size ranges from a few millimeters to several centimeters. Multiple jaw osteomas are a common feature of Gardner syndrome.
Gardner syndrome: osteoma of the mandible.
Laboratory tests Histopathological examination, radiography.
Differential diagnosis Exostoses, osteosarcoma.
Treatment Surgical excision.

Osteosarcoma
Definition Osteosarcoma is the most common primary malignant neoplasm of bone.
Etiology Unknown.
Clinical features
The jaws are affected in 6–7% of cases, and usually during the third decade of life. Both jaws are affected equally and it is more common in men. Clinically, the lesion presents as a rapidly growing hard swelling that progressively produces facial deformity. Pain, paresthesia, tooth loosening, and nasal obstruction may also occur.
Osteosarcoma of the upper jaw, presenting as a hard swelling.
Laboratory tests Histopathological examination, radiography, CT scans.
Differential diagnosis Chondrosarcoma, Ewing sarcoma, metastatic tumors, odontogenic tumors and cysts, giant-cell tumor.
Treatment Surgical excision and supplementary radiotherapy and chemotherapy.

Chondrosarcoma
Chondrosarcoma  is more common in men than in women, between 30 and 60 years of age. Clinically, it appears as a painless hard swelling that progressively enlarges, causing extensive bone destruction with pain and loosening of the teeth.

Burkitt Lymphoma
Definition Burkitt lymphoma is a high-grade malignant B-lymphocyte lymphoma.
Etiology Epstein–Barr virus is closely associated.
Clinical features
The malignancy is prevalent in central Africa (the endemic form), and usually affects children 2–12 years of age. Cases have also been observed in other countries (the nonendemic form), and recently in patients with AIDS. The jaws are the most common site of lymphoma (60–70%). Clinically, it presents as a rapidly growing hard swelling that causes bone destruction, tooth loss, and facial deformity.Pain, paresthesia and large ulcerating or nonulcerating masses may also be seen.
Burkitt lymphoma, facial deformity.
Burkitt lymphoma, gingival mass
Burkitt lymphoma on the gingiva in a young patient with AIDS
Laboratory tests Histopathological examination, radiography.
Differential diagnosis Central giant-cell granuloma, ossifying fibroma, other non-Hodgkin lymphomas, and odontogenic tumors.
Treatment Chemotherapy, radiotherapy.

Multiple Myeloma
Definition Multiplemyeloma is a relatively rare malignant plasma-cell disorder.
Etiology Unknown.
Clinical features The malignancy is more common in men over 50 years of age, and the jaws are affected in about 30% of cases. Clinically, it presents with bone swelling, tooth mobility, pain, and paresthesia. A painless soft swelling, usually on the alveolar mucosa and gingiva, may develop as part of the overall disease spectrum.
Multiple myeloma, swelling on the gingiva
Laboratory tests Bone-marrow biopsy, radiography, serum and urine protein electrophoresis.
Differential diagnosis Plasmacytoma, non-Hodgkin lymphoma, Ewing sarcoma, leukemia, Langerhans cell histiocytosis.
Treatment Chemotherapy, radiotherapy.

Paget Disease
Definition Paget disease, or osteitis deformans, is a chronic, relatively common disorder characterized by uncoordinated bone resorption and deposition.
Etiology Unknown.
Clinical features Clinically, the signs and symptoms develop gradually and are characterized by bone pain, headache, deafness, visual disorders, dizziness, and progressive bone enlargement. Progressive expansion of the maxilla and the mandible lead to symmetrical thickening of the alveolar ridges.
Paget disease, enlarged maxilla
Edentulous patients may complain that their dentures do not fit due to alveolar enlargement.
Paget disease, alveolar enlargement
Delayed wound healing, bleeding, and osteomyelitis after tooth extraction may occur. The maxilla is more frequently affected than the mandible. Malesare more often affected than females. Two major forms of the disease are recognized: (a) the monostotic, and (b) the polyostotic. The clinical diagnosis should be confirmed by a histopathological and radiographic examination. Elevations of serum alkaline phosphatase and urinary hydroxyproline levels are common findings.
Differential diagnosis Fibrous dysplasia, osteosarcoma, multiple exostoses, fibro-osseous lesions.
Treatment Most cases require no treatment. Calcitonin and bisphosphonates may slow the pathological process.

Odontogenic Tumors
Definition Odontogenic tumors are a group of lesions that originate from odontogenic epithelium and ectomesenchyme.
Etiology Unknown. Some are neoplasms and others hamartomas.
Classification On the basis of the tissue of origin, three major varieties are recognized: (a) tumors of odontogenic epithelium, (b) tumors of odontogenic ectomesenchyme, and (c) mixedod ontogenic tumors.
Clinical features Most odontogenic tumors are usually asymptomatic for long time and are discovered only during a routine radiographic examination. However, with time they may form a usually painless slow-growing swelling or expansion of the mandible or the maxilla.
Odontogenic myxoma, expansion of the retromolar area
Extraosseous calcifying epithelial odontogenic tumor presenting as a gingival mass
The clinical signs and symptoms are not diagnostic and the final diagnosis should be made by radiographic and histopathological examinations.
Differential diagnosis Different varieties of odontogenic tumors, odontogenic cysts, osteosarcomas, chondrosarcomas, multiplemyeloma.
Treatment Surgical excision.

Wednesday, November 2, 2011

A Note on Ameloblastoma: pathogenesis, signs & symptoms, Radiographic features & subtypes...etc


Ameloblastoma
Historically, ameloblastoma has been recognized for over a century and a half. Its frequency, persistent local growth, and ability to produce marked deformity before leading to serious debilitation probably account for its early recognition. Recurrence, especially after conservative treatment, has also contributed to the awareness of this lesion.

Pathogenesis 
This neoplasm originates within the mandible or maxilla from epithelium that is involved in the formation of teeth. Potential epithelial sources include the enamel organ, odontogenic rests (rests of Malassez, rests of Serres), reduced enamel epithelium, and the epithelial lining of odontogenic cysts, especially dentigerous cysts. The trigger or stimulus for neoplastic transformation of these epithelial residues is totally unknown.

Mechanisms by which ameloblastomas gain a growth and invasion advantage include overexpression of anti-apoptotic proteins (Bcl-2, Bcl-xL) and interface proteins (fibroblast growth factor [FGF], matrix  metalloproteinases [MMPs]). Ameloblastomas, however, have a low proliferation rate. Mutations of the p53 gene do not appear to play a role in the development or growth of ameloblastoma.

Signs & symptoms
  • Occurs predominantly in the fourth and fifth decades of life
  • Appears to be no gender predilection (Slightly more in males)
  • Mandibular molar-ramus area is the most favored site
  • Slowly growing,
  • Painless,
  • Hard bony swelling or expansion of jaw,
  • Thinning of cortical plates produces “Egg shell crackling”.
  • Other symptoms – Tooth mobility, root resorption and paresthesia if inferior alveolar nerve is affected.

RADIOLOGICAL FEATURES
  • Typically rounded
  • Radiographic margins are usually well defined and sclerotic
  • Multilocular radiolucency
  • Scalloped margins
  • When loculations are large, the appearance is called as “SOAP BUBBLE” appearance
  • When loculations are smaller, the appearance is called “HONEY COMBED” appearance.
  • Buccal & lingual cortical plates are expanded.
  • Roots of adjacent teeth displaced / resorbed.
  • As it spreads through medullary spaces, radiographic margins are not accurate indication of bone involvement.
  • Desmoplastic ameloblastoma, also has a predilection for the anterior jaws and radiographically resembles a fibroosseous lesion (mixed radiopaque-radiolucent)

DIFFERENTIAL DIAGNOSIS
  • ODONTOGENIC KERATOCYST
  • FIBROUS DYSPLASIA
  • OSSIFYING FIBROMA
  • CENTRAL GIANT CELL GRANULOMA

BIOLOGIC SUBTYPES
  •         Solid/Multicystic Ameloblastoma
  •         Unicystic Ameloblastoma
                        Luminal
Tumor is confined to luminal surface of cyst.
Seen as fibrous cyst wall with lining comprised totally / partially of ameloblastic epithelium, showing a basal layer of columnar / cuboidal reversely polarized cells.
Overlying epithelial cells are loosely adhesive, resembling the stellate reticulum of dental organ.
                        Intraluminal
This variant shows the tumor from cyst lining protruding into the lumen of cyst.
Intraluminal projections resemble plexiform ameloblastoma in most cases, though not always. 
                        Mural

In this type, the fibrous wall of the cyst is infiltrated with typical follicular / plexiform ameloblastoma.
      Believed to be more aggressive than other two variants
  •         Desmoplastic Ameloblastoma
  •         Peripheral Ameloblastoma

  •         Malignant Ameloblastoma
  •         Ameloblastic carcinoma   


HISTOPATHOLOGICAL SUBTYPES OF SOLID AMELOBLASTOMA
    1. FOLLICULAR
Islands of epithelium resemble dental organ surrounded by mature connective stroma.
Individual follicles show central mass of stellate reticulum like cells surrounded by a single peripheral layer of ameloblast like cells.
Nuclei of peripheral cells are reversely polarized.
       Within the islands, cyst formation is common.

    1. PLEXIFORM
Instead of islands, long, anastomosing cords and occasional sheets of epithelial cells bounded by columnar / cuboidal cells.
Cells within cords are more loosely arranged than peripheral cells.
Supporting stroma is loose and vascular.
      Cyst formation occurs, not inside follicles, but in surrounding stroma.

    1. ACANTHOMATOUS
Central area of follicles show extensive squamous metaplasia, often associated with keratin formation.
DOEAS NOT INDICATE A MORE AGGRESSIVE COURSE OF TUMOR.
Can be confused with squamous cell carcinoma.

    1. GRANULAR CELL
Follicles / sheets of cells show granular cell change.
These cells have abundant cytoplasm filled with eosinophilic granules.
Seen in younger persons and appears to be more aggressive clinically.

    1. BASAL CELL TYPE
Least common type
Composed of nests / sheets of hyperchromatic basaloid cells
No stellate reticulum present centrally and peripheral cells tend to be cuboidal rather than tall columnar

TREATMENT
  • Can vary from simple enucleation to curettage to en bloc resection.
  • As lesion spreads through medullary spaces, simple enucleation can leave islands of tumor within the jaws, leading to recurrence.
  • Marginal resection is the optimal method.
  • Rarely can undergo malignant transformation.


Monday, October 24, 2011

A NOTE ON DISEASES CLINICALLY PRESENTING AS DESQUAMATIVE GINGIVITIS


DISEASES CLINICALLY PRESENTING AS DESQUAMATIVE GINGIVITIS
Lichen Planus
Lichen planus is a relatively common, chronic, dermatosis characterized by the presence of cutaneous   violaceous papules that may coalesce to form plaques. The current evidence suggests that lichen planus is an immunologically mediated mucocutaneous disorder where host T lymphocytes play a central role . Although the oral cavity may present lichen planus lesions with a distinct clinical configuration and distribution, the clinical presentation sometimes may simulate other mucocutaneous disorders. Therefore a clinical diagnosis of oral lichen planus should be accompanied by a broad differential diagnosis. Numerous epidemiologic studies have shown that oral lichen planus presents in 0.1% to 4% of the population." The majority of patients with oral lichen planus are middle-aged and older females with a 2:1 ratio of females to males. Although possible, children are rarely affected. In a dental setting, cutaneous lichen planus is observed in about one third of the patients diagnosed with oral lichen planus.  In contrast, two thirds of patients seen in dermatologic clinics exhibit oral lichen planus.
Oral Lesions
Although there are several clinical forms of oral lichen planus (reticular, patch, atrophic, erosive and bullous), the most common are the reticular and erosive subtypes. The typical reticular lesions are asymptomatic, bilateral, and consist of interlacing white lines on the posterior region of the buccal mucosa. The lateral border and dorsum of the tongue, hard palate, alveolar ridge, and gingiva may also be affected. In addition, it is not unusual for the reticular lesions to have an erythematous background, a feature that is associated with the coexistence of candidiasis. Oral lichen planus lesions follow a chronic course and have alternating, unpredictable periods of quiescence and flares.
The erosive subtype of lichen planus is often associated with pain and clinically manifests as atrophic, erythematous areas. Fine white radiating striations are observed bordering the atrophic zones. These areas may be sensitive to heat, acid, and spicy foods.
Gingival Lesions
Up to 10% of patients with oral lichen planus have lesions restricted to the gingival tissue that may occur as one or more types of four distinctive patterns:
1. Keratotic lesions. These raised white lesions may present as groups of individual papules, linear or reticulate lesions, or plaquelike configurations.
2. Erosive or ulcerative lesions. These extensive erythematous areas with a patchy distribution may present as focal or diffuse hemorrhagic areas. These lesions are exacerbated by slight trauma (e.g., toothbrushing).
3. Vesicular or bullous lesions. These raised, fluid-filled lesions are uncommon and short lived on the gingiva, quickly rupturing and leaving an ulceration.
4. Atrophic lesions. Atrophy of the gingival tissues with ensuing epithelial thinning results in erythema confined to the gingiva.

Histopathologic, Direct, and Indirect Immunofluorescence Findings in Selected Conditions That May Present Clinically as Desquamative Gingivitis

     Disease

     Histopathology
            Direct Immunofluorescence
Indirect
Immunofluorescence
Biopsy Perilesional
Mucosa
Biopsy Uninvolved
Mucosa
Pemphigus
Intraepithelial clefting
above the basal cell
layer. The basal cells
have a characteristic
"tombstone" appear-
ance. Acantholysis is
present.
Intercellular deposits in epithelium; IgG
in all cases, C3 in most cases.
Same as perilesional
mucosa.
Intercellular (IgG) anti-
bodies in >90% of
cases.
Cicatricial
pemphigoid
Subepithelial clefting
with epithelial separation from the underlying lamina propria, leaving an intact basal layer.
Linear deposits of
C3, with or without
IgG at the basement
membrane zone in
almost all cases.
Same as perilesional
mucosa.
Basement membrane zone (IgG) antibodies in 10% of cases.
Bullous
pemphigoid
Subepithelial clefting
with epithelial separa-
tion from the under-
lying lamina propria,
leaving an intact basal
layer.
Linear deposits of
C3, with or without
IgG at the basement
membrane zone in
almost all cases.
Same as perilesional
mucosa.
Basement membrane zone (IgG) antibodies in 40% to 70% of cases.
Epidermolysis
bullosa
acquisita
Similar to bullous and
cicatricial pemphigoid.
Linear deposits of
IgG and C3 at the
Basement membrane zone in almost all cases.
Same as perilesional
mucosa.
Basement membrane zone (IgG) antibodies in 25% of cases.
Lichen planus
Hyperkeratosis, hydropic degeneration of the basal layer, "saw-toothed" rete pegs.
The lamina propria
exhibits a dense, band-
like infiltrate primarily
of T lymphocytes. Colloid bodies are present.

Fibrilar deposits
of fibrin at the
dermal-epiderma
junction.
     



      Negative




   Negative
Chronic
ulcerative
stomatitis
Similar to erosive lichen planus
(hype rkeratosis,
acanthosis, basal cell
layer liquefaction, sub-
epithelial clefting, and
lympho-histiocytic
chronic infiltrate in a
bandlike configuration.

IgG deposits in nuclei of basal layer epithelial cells.

Same as perilesional
mucosa.
ANA specific for basal cells of stratified squamous epithelium.
Linear IgA
disease
Similar to erosive lichen planus.
Linear deposits of IgA at the basement membrane zone.
Same as perilesional
mucosa.
IgA basement membrane zone (IgA) antibodies in 30% of cases.
Dermatitis
herpetiformis
Collection of neutro-
phils, eosinophils, and
fibrin in connective
tissue papillae.
IgA deposits in
dermal papillae
in 85% of cases.
IgA deposits in dermal papillae in 100% of cases.
IgA endomysial antibodies in 70% of cases, gliadin antibodies in 30% of
cases.
Systemic lupus
erythematosus
Hyperkeratosis, basal
cell degeneration,
epithelial atrophy,
and perivascular
inflammation.
I g (G or M), with or without C3 deposits at dermal-epidermal
junction.
Same as perilesional
mucosa.
ANA in more than 95% of cases, DNA and ENA
antibodies in more than 50% of cases.
Chronic cutaneous lupus
erythematosus
Hyperkeratosis, basal
cell degeneration,
epithelial atrophy,
and perivascular
inflammation.
Ig (G or M), with or without C3 deposits at dermal-epidermal
junction.
 
       Negative

   Usually negative
Subacute lupus
erythematosus
Less inflammatory cell
infiltrate than systemic
and chronic cutaneous
lupus erythematosus
but with similar
microscopic features.
Ig (G or M), with or without C3 deposits at dermal-epidermal
junction in 60% of cases; granular IgG deposits in basal cell cytoplasm in 30% of cases.

Same as perilesional
mucosa.

ANA in 60% to 90%, SS-A(Ro) in 80%, RF in 30%, and RNP in 10% of cases.


Gingivitis: clinical features. A, Localized, diffuse, intensely red area facial of tooth #7 and dark pink marginal changes in the remaining anterior teeth. B, Generalized papillary gingivitis. C, Generalized marginal inflammatory lesion. D, Generalized diffuse inflammatory lesion. E, Papillary gingival enlargement. F, Different degrees of recession. Recession is slight in teeth #26 and 29 and marked in #27 and 28.
Note the irregular contours of the gingiva in #28 and the lack of attached gingiva in #27. G, Insertion of a probe into the gingival sulcus.
Note the lack of stippling, the slightly rolled margins, and the dark red color. H, Bleeding appears about 30 seconds after probing.

A, Necrotizing ulcerative gingivitis: typical punched out interdental papilla between mandibular canine and lateral incisor. B, Necrotizing ulcerative gingivitis: typical lesions with progressive tissue destruction. C, Necrotizing ulcerative gingivitis: typical lesions with spontaneous hemorrhage. D, Necrotizing ulcerative gingivitis: typical lesions producing irregular gingival contour. E, Primary herpetic gingivostomatitis: typical diffuse erythema. F, Primary herpetic gingivostomatitis: vesicles on the gingiva.
Erosive lichen planus presenting as desquamative gingivitis. The gingival tissues are erythematous, ulcerated, and painful.
Gingival mucous membrane pemphigoid. Lesions of cicatricial pemphigoid confined to the gingival tissues, producing a typical desquamative gingivitis appearance.
Pemphigus vulgaris of the gingiva. Clinical appearance of a patient with pemphigus vulgaris presenting oral lesions confined to the gingiva. The clinical diagnosis was consistent with desquamative gingivitis.
Pemphigus vulgaris of the oral cavity. Multiple and coalescent areas of ulceration covered by necrotic epithelium. This patient presented with large ulcers in the labial mucosa, tongue, and soft palate.
Chronic ulcerative stomatitis. Erythema and ulceration of the gingiva consistent with a clinical diagnosis of desquamative gingivitis.
Linear IgA. Intense erythema and ulceration of the gingiva consistent with desquamative gingivitis.
Lupus erythematosus of the oral cavity presenting as desquamative gingivitis. Intense erythema with ulceration bordered by white radial lines.
Plasma cell gingivitis. The gingiva presents a band of moderate to severe inflammation reminiscent of desquamative gingivitis.
Graft versus host disease in a recipient of an allogenic bone marrow transplant. The maxillary gingiva exhibits features consistent with desquamative gingivitis.
Wegener's granulomatosis affecting the gingi-val tissues. The classic "strawberry gums" appearance of the mandibular gingiva is seen in this patient. A slight resemblance with desquamative gingivitis is evident.
Erythema multiforme. Large, shallow, and painful ulcers involving the labial and buccal mucosae. Hemorrhagic crusting of the mandibular vermilion border of the lips is observed.

Treatment of lichen planus.
 Treatment of pemphigus vulgaris.
Treatment of cicatricial pemphigoid.

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