Ps. This is a good case report on Chondroectodermal dysplasia – https://api.semanticscholar.org/CorpusID:5721166
Sources – Shafer’s textbook of oral pathology
Image reference – Shafer’s textbook of oral pathology , semanticscholar.org
Category: Oral Pathology
MANAGEMENT: TMJ ANKYLOSIS
- Ankylosis can ONLY be treated surgically.
- There is no form of pharmacological management.
- Type of surgery depends on age of the patient & extent of deformity.
- Treatment also varies if ankylosis is unilateral/bilateral.
SINGLE STAGE V/S 2-STAGE SURGICAL PROCEDURES:
- Surgery can be done in two stages.
- In the first operation, only a release of ankylosis is done.
- It is believed that growth takes place after release of ankylosis.
- Second stage procedure,an orthognathic surgery can be performed to restore esthetics.
- Some, however prefer to it as a single stage procedure,where release of ankylosis + esthetic correction is done in a single stage operation in adults.
SURGICAL PROCEDURES:
There are 3 types:
- Condylectomy.
- Gap Arthroplasty.
- Interpositional Arthroplasty.
TMJ APPROACHES:
P1 and P2— preauricular approaches;
PA-postauricular approach;
I—inverted hockey stick approach;
E -endaural approach.
R-retromandibular approach.
1. CONDYLECTOMY:
2. GAP ARTHROPLASTY:
3. INTERPOSITIONAL ARTHROPLASTY:
KABAN’S PROTOCOL:
REFERENCES:
- Textbook of Oral & Maxillofacial Surgery, Chitra Chakravarthy (2nd Edition)
- interchopen.com
- researchgate.net
ANKYLOSIS OF TMJ
CLASSIFICATION:
1. Based on type of tissue causing Ankylosis:
2. Based on the Side Involved :
- Unilateral Ankylosis
- Bilateral Ankylosis
3. Based on Severity of Ankylosis:
- Partial
- Complete
4. Based on Etiology of Trismus:
- Pseudo Ankylosis
- True Ankylosis
SAWHNEY’S CLASSIFICATION:
CLINICAL FEATURES:
INVESTIGATIONS:
1. Radiographs:
– OPG
-PA VIEW:
– Lateral Oblique View of Mandible:
Ankylotic mass can seen in the Anteroposterior direction.
2. Lateral Cephalogram:
3. CT Scan:
Helpful as it gives an accurate picture of proximity of ankylotic mass to important structure,that cannot be seen in a radiograph.
RADIOGRAPHIC FEATURES:
- Decreased ramus height on the affected site.
- Lack of joint space.
- Normal joint space obliteration by bone/fibrous growth.
- Elongation of coronoid process.
- Deep antigonial notch.
REFERENCES:
- Textbook of Oral & Maxillofacial Surgery, Chitra Chakravarthy (2nd Edition).
- DentalHypothesis.com
- Europe PMC
- PocketDentistry.com
- SciELO.com
LUDWIG`S ANGINA
LUDWIG`S ANGINA
REFERENCES:
- Textbook of Oral & Maxillofacial Surgery,Chitra Chakravarthy (2nd Edition)
- AAFP.org
- orosurgery.com
- seminarscholar.com
- craighospital.com
Squamous cell carcinoma
Oral cancer is a disease with very poor prognosis because it is not recognised and treated when small and early.
INCIDENCE.
-Squamous cell (epidermoid) carcinoma comprises 90% of all oral malignant tumours and 5% of all human malignancies.
-The peak incidence in the UK and the USA is from 55 to 75 years of age, whereas in India it is from 40 to 45 years of age.
-Oral cancer is a very frequent malignancy in India, Sri Lanka and some Eastern countries, probably related to habits of betel-nut chewing and reversed smoking .
– There is a definite male preponderance.
-It can occur anywhere in the mouth but certain sites are more commonly involved.
-These sites, in descending
order of frequency, are: the lips (more commonly lower),
tongue, anterior floor of mouth, buccal mucosa in the region
of alveolar lingual sulcus, and palate.
ETIOLOGY.
As with other forms of cancer, the etiology of squamous cell carcinoma is unknown. But a number of etiological factors have been implicated:
Strong association:
i) Tobacco smoking and tobacco chewing causing leukoplakia is the most important factor .
ii) Chronic alcohol consumption.
iii) Human papilloma virus infection, particularly HPV 16, 18 and 33 types.
Weak association:
i) Chronic irritation from ill-fitting denture or jagged teeth.
ii) Submucosal fibrosis as seen in Indians consuming excess of chillies.
iii) Poor orodental hygiene.
iv) Nutritional deficiencies.
v) Exposure to sunlight (in relation to lip cancer).
vi) Exposure to radiation.
vii) Plummer-Vinson syndrome, characterised by atrophy
of the upper alimentary tract.
The most common molecular alterations in oncogenes
seen in squamous cell carcinoma of the oral cavity are in
p16, p53, cyclin D, p63, PTEN, and EGFR.
MORPHOLOGIC FEATURES.
Grossly, squamous cell carcinoma of oral cavity may have the following types
i) Ulcerative type—is the most frequent type and is
characterised by indurated ulcer and firm everted or
rolled edges.
ii) Papillary or verrucous type—is soft and wart-like growth.
iii) Nodular type—appears as a firm, slow growing submucosal nodule.
iv) Scirrhous type—is characterised by infiltration into
deeper structures.
*All these types may appear on a background of leukoplakia or erythroplasia of the oral mucosa.
Enlarged cervical lymph nodes may sometimes be present.
Histologically.
– squamous cell carcinoma ranges from well-differentiated keratinising carcinoma to highly undifferentiated neoplasm . -Changes of epithelial dysplasia are often present in the surrounding
areas of the lesion.
–Carcinoma of the lip and intraoral squamous carcinoma are usually always well-differentiated
source -textbook of pathology for dental students harsh mohan
BULLOUS PEMPHIGOID
A chronic, autoimmune, sub-epidermal blistering skin disease that rarely involves mucous membrane.
🔹Clinical Features:
Age: Elderly (>60 years)
Skin Lesions:
- Generalised non-specific rash, commonly on Limbs.
- Appears urticarial/eczematous; persist for several weeks to months.
- Vesicles & bullae arise in prodromal skin lesion as well as Normal skin.
- The blisters are thick walled and don’t rupture easily.
- ruptured blisters are usually sensitive and painful, have raw eroded area which heals rapidly.
Oral Manifestations:
Vesicles appear gingivally👇🏻
Erythematous & desquamate as result of minor frictional trauma
👉🏻 Oral lesions comprise of bullae/vesicle that rupture to form erosions and ultimately leave out ulcerations
👉🏻 Other sites:
- Buccal Mucosa
- Tongue
- Floor of the mouth
- Palate
🔹Diagnosis:
Apart from evaluating history, clinical presentation, histopathological analysis is carried out followed by direct immunofluorescence study for the differential diagnosis and confirmation of the condition.
👉🏻Histopathology:
- Acanthotic mucosa
- Subepidermal non-specific vesicles with fibrous exudate
👉🏻Direct immunofluorescence is found to be the gold standard test. Deposition pattern of different types of immunoreactants differentiates the various immune-mediated diseases. Direct immunofluorescence shows presence of IgG and C3 deposits along the basement membrane zone.
👉🏻Electron Microscopy: In bullous pemphigoid (BP), the 180 kD antigen (BPAG2) was shown by immuno-EM to be a transmembrane molecule and to possess an autoantibody binding site outside the cell, suggesting a major pathogenic role for the BPAG2 in blister formation.
🔹Differential Diagnosis:
• Mucous membrane pemphigoid can be differentiated from BP by its predominant involvement of mucosal surfaces and positive Nikolsky’s sign.
• Lichen planus pemphigoides is clinically differentiated by the presence of lichen planus lesions in addition to tense blisters.
• Nikolsky’s sign is present in case of pemphigus and cicatricial pemphigoid, but not in the case of BP.
🔹 Treatment:
👉🏻Treatment is based on the degree of cutaneous and oral involvement. Mostly, topical steroid (clobetasol propionate) gives satisfactory result in case of smaller area of skin involvement, whereas larger area of skin involvement and recurrent cases are treated satisfactorily with systemic steroids and immunosuppressive agents.
👉🏻Recommended dosage for oral prednisolone is 0.3–1.25 mg/kg body weight/day, controls disease within 1–2 weeks, followed by which the dose is tapered. Dexamethasone (100 mg in 500 mL 5% dextrose i.v. over 2–3 h for three consecutive days) is the preferred steroid for pulse therapy, either administered alone or in combination with cyclophosphamide.
Other drugs for treating BP include new antibody modulators, rituximab 375mg/m2weekly over 4 weeks and omalizumab subcutaneously 300–375 mg for every 6 weeks.
👉🏻Higher doses of systemic corticosteroids seem to be associated with higher mortality rates, which led to the addition of corticosteroid-sparing agents to the treatment of BP. The most frequently used immunosuppressive agent is azathioprine (0.5–2.5 mg/kg body weight/day). Others being cyclophosphamide, methotrexate, cyclosporine A, combination tetracycline/minocycline along with nicotinamide, and more recently, mycophenolate mofetil, a DNA synthesis inhibitor, and methotrexate, a folate antagonist.
👉🏻IVIg – A dose of 1–2 g/kg for five consecutive day cycle of 0.4 g/kg/day, although a 3-day cycle may be used in cases that are nonresponsive to conventional therapy.
Dr. Mehnaz Memon🖊
References:
- http://www.jiaomr.in/article.asp?issn=0972-1363;year=2018;volume=30;issue=4;spage=432;epage=435;aulast=Aparna
- https://www.cidjournal.com/article/S0738-081X(00)00178-4/abstract
- Shafer’s Textbook of Oral Pathology, 7th edition
Oral Leukoplakia
DEFINITION- Leukoplakia (white plaque) may be clinically
defined as a white patch or plaque on the oral mucosa, exceeding 5 mm in diameter, which cannot be rubbed off nor can be classified into any other diagnosable disease.
–the term ‘leukoplakia’ is reserved for epithelial thickening which may range from completely benign to atypical and to premalignant cellular changes.
INCIDENCE–
1. It occurs more frequently in males than
females.
2.The lesions may be of variable size and appearance.
3. The sites of predilection, in descending orderof frequency, are: cheek mucosa, angles of mouth, alveolar mucosa, tongue, lip, hard and soft palate, and floor of the mouth.
4.In about 4-6% cases of leukoplakia, carcinomatous
change is reported.
ETIOLOGY-
1. It has the strongest association with the use of tobacco in various forms, e.g. in heavy smokers (especially in pipeand cigar smokers) and improves when smoking is discontinued, and in those who chew tobacco as in paan, paan masaala, zarda, gutka etc.
2.The condition is also known by other names such as smokers keratosis and stomatitis nicotina.
3. Other etiological factors implicated are chronic friction such as with ill-fitting dentures or jagged teeth, and local irritants like excessive consumption of alcohol and very hot and spicy foods and beverages.
4. A special variety of leukoplakia called ‘hairy leukoplakia’ has
been described in patients of AIDS and has hairy or corrugated surface but is not related to development of
oral cancer.
MORPHOLOGIC FEATURES.
1.Grossly, the lesions of leukoplakia may appear white, whitish-yellow, or redvelvety of more than 5 mm diameter and variable in appearance.
2. They are usually circumscribed, slightly elevated, smooth or wrinkled, speckled or nodular.
Histologically, leukoplakia is of 2 types:
- The hyperkeratotic type- This is characterised by an orderly and regular hyperplasia of squamous epithelium with hyperkeratosis on the surface.
- Dysplastic type- When the changes such as irregular stratification of the epithelium, focal areas of increased and abnormal mitotic figures, hyperchromatism, pleomorphism, loss of polarity and individual cell keratinisation are present, the lesion is considered as epithelial dysplasia
-The subepithelial tissues usually show an inflammatory infiltrate composed of lymphocytes and plasma cells.
– The extent and degree of the epithelial changes indicate the degree of severity of the epithelial dysplasia.
-Usually, mild dysplasia may revert back to normal if the offending etiologic factor is removed, whereas severe dysplasia indicates that the case may progress to carcinoma.
source – textbook of pathology for dental students harsh mohan
Achondroplasia
Lumbar lordosis 
Mandibular prognathism 
Peter Dinklage , who played Tyrion Lanister in the epic “Game of thrones” is suffering from achondroplasia.
Sources – Anil Ghoms textbook of oral medicine , osmosis.org
Image source – researchgate.net , Google images
PATHOGENESIS OF FIBROUS DYSPLASIA
APERT SYNDROME
🔖 Acrocephalosyndactyly. The condition is autosomal dominant i.e, one copy (out of 2) of the defective gene is sufficient to cause the abnormality in the offspring.
🔹Characteristics:
- Craniosynostosis (premature fusion of the skull bones)
- Craniofacial anomalies
- Syndactyly (Fusion of fingers and toes)
🔹Etiology:
🔹What are the Symptoms and Signs of Apert Syndrome?
The various clinical features include:
- Asians affected
- Acrocephaly, Brachycephaly, flat occiput & prominent forehead.
- Late closing fontanels
- Low set ears, hearing loss
- Eyes: Down slanting of palpebral fissures, Widely spaced eyes(Hypertelorism), Shallow orbits, Abnormally bulging eyes (Exophthalmos)
- Nose: Depressed Nasal bridge, short, wide with bulbous tip, Parrot beaked appearance, Atresia
- Jaw:
- Prominent Mandible
- Maxillary hypoplasia
- Drooping angles of mouth
- High arched palate
- Bifid uvula
- Cleft palate
- Crowded upper teeth
- Malocclusion
- Delayed & ectopic eruption
- Shovel shaped incisors
- Supernumerary teeth
- V-shaped maxillary dental arch
- Bulging alveolar ridges
8. Partial to complete fusion of digits: 2-4th digits – MITTEN HANDS & SOCK FEET; Sole – supinated
9. Intelligence – Normal
10. ⬆️ intracranial pressure – optic atrophy, papilledema
11. Hyperhidrosis
12. Cardiovascular system: Atrial Septal defect, Ventricular septal defect, Patent ductus Arteriosus
🔹How do you Treat Apert Syndrome?
Standard Therapies
The treatment of Apert syndrome aims at addressing the specific symptoms that may be present in the particular individual. Treatment is usually symptomatic and supportive.
- Craniosynostosis and associated hydrocephalus in some cases may give rise to an abnormally increased pressure within the skull (intracranial pressure) and on the brain. In these cases, early surgery (within 2 to 4 months after birth) becomes necessary to correct the defects in the skull and facial bones.
- Insertion of a tube (shunt) to drain excess cerebrospinal fluid (CSF) away from the brain and into another part of the body like the abdomen where the CSF can be absorbed can be done to relieve associated hydrocephalus (fluid accumulation in the brain).
- Early repair and reconstructive surgery may also be done in some infants with Apert syndrome to address craniofacial abnormalities.
- Other defects such as those of heart, eye and ear defects may also need correction.
Dr. Mehnaz Memon🖊
References:
- https://www.medindia.net/amp/patientinfo/apert-syndrome.htm
- Shafer’s textbook of Oral Pathology – 7th Ed.
Dentowesome 