Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Oral Medicine > Year 3 > Flashcards

Year 3 Flashcards

1
Q

What are the organic causes of xerostomia?

A
  1. Sjögren’s syndrome
  2. Irradiation
  3. Transient mumps (viral infection that leads to swelling of parotid glands)
  4. HIV infection
  5. HCV infection
  6. Sarcoidosis (small granulomas developing in organs of the body)
  7. Amyloidosis (disease caused by deposition of abnormal protein ‘Amyloid’ in tissues and organs through out the body)
  8. Iron deposition;
    a. Haemotochromosis (slow build up of iron levels in the body)
    b. Thalassaemia (abnormal formation of Haemoglobin leading to impaired RBC function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What are the drugs associated with xerostomia?

A
  1. Diuretic overdose
  2. Drugs with antimuscarinic effect
  3. Tricyclics and some other anti depressants
  4. Antihistamines
  5. Antiemetics (used for nausea and vomiting)
  6. Antipsychotics (particularly phenothiazines)
  7. Some older antihypertensives (ganglion blocker and clonidine)
  8. Drugs with sympathomimetic actions
  9. Cold cures with ephedrine
  10. Decongestant
  11. Bronchodilators
  12. Appetite suppressant (particularly amphetamines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are functional causes of xerostomia?

A
  1. Dehydration
  2. Fluid deprivation or loss
  3. Haemorrhage
  4. Persistent diarrhoea/vomiting
  5. Phycogenic
    a. Anxiety states
    b. Depression
  6. Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define signs and symptoms

A

Symptoms; subjective evidence of the disease (what the patient complains of)
Signs; an objective physical finding (what the clinician finds upon examining the patient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are symptoms of xerostomia?

A
  1. Dry mouth
  2. Difficulty swallowing
  3. Difficulty eating
  4. Difficulty speaking
  5. Difficulty wearing dentures
  6. Mucosal stick to each other and the teeth
  7. Bad taste in the mouth
  8. Halitosis
  9. Sore mouth
  10. Deteriorating dentition
  11. Swelling of the salivary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the signs of xerostomia?

A
  1. Salivary gland enlargement
  2. Mucosa sticks to dental mirror
  3. Consistency of saliva is stringy, frothy and thick
  4. Little or no pooling of saliva in floor of mouth
  5. Lobulated tongue
  6. Shiny mucosa
  7. Food debris
  8. Plaque accumulation
  9. Depapillated tongue (tongue becomes smooth)
    Additional findings;
  10. Evidence of candidiasis (angular cheilitis, erythematous mucosa, thrush, denture stomatitis)
  11. Smooth surface caries
  12. Traumatic ulceration (patient accidentally biting their cheeks)
  13. Poor denture retention
  14. Bacterial sialadenitis (infection and inflammation of salivary glands)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are developmental causes of xerostomia?

A
  1. Aplasia (problems with glands); most likely to occur brought developmental defects and malformation of 1st and 2nd brachial arches. Eg; parotid gland aplasia in Treacher Collins syndrome
  2. Atresia (problems with ducts); congenital absence or narrowing of a duct which causes distension in the gland and atrophy (wasting away of the gland)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is sialometry?

A

Sialometry is the objective evidence of reduced unstimulated salivary flow rate.

  1. Whole saliva
  2. 15 mins (ideal)
  3. 5 mins (clinical reality)
  4. Normal; 0.3 - 0.4ml/min
  5. Significant reduced rate; <0.1ml/min
  6. Stimulated sialometry is done with sugar free gum or saliva stimulating tablet (x10 of unstimulated); 1-2ml/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is sialography?

A

Sialography is an imaging technique used to demonstrate the ductal system of the parotid/submandibular

  1. It involves the introduction of a radiopaque contrast medium into the orifice of one of the major salivary glands via a catheter
  2. Radiographs (usually lateral obliques) are taken before and after the catheter is inserted
  3. These determine the flow of fluid and examine the drainage of the fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Schirmer test?

A

It is the objective evidence of the normal functioning of lacrimal glands (whether it produces enough tears to keep the eyes moist)

  1. The test uses paper strips (with rose Bengal die) inserted under the lower eyelid for 5 mins to measure tear production
  2. The amount of moisture on the paper is then measured
  3. Normal; more than 15mm
  4. Mild; 14-9mm
  5. Moderate; 8-4mm
  6. Severe; less than 4mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is scintigraphy?

A

Scintigraphy is an objective evidence of salivary gland function

  1. Technetium pertechnetate is intravenously injected and taken up by the salivary glands
  2. Scanning of the salivary gland is carried out every 30s
  3. Salivary gland function is then assessed with computer-assisted quantitative programmes
  4. This test is beneficial for comparing diseased gland with remaining healthy gland or to detect generalised loss of glandular function (especially useful for diagnosis of Sjögren’s syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are complications of xerostomia?

A
  1. Caries
  2. Candidosis
  3. Halitosis
  4. Sialadenitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which gland contributes to unstimulated and stimulated salivary flow rate (respectively)?

A 
Unstimulated salivary flow rate
1. 65% from submandibular gland
2. 15-20% from parotid gland
3. 7-8% from sublingual and minor glands
Stimulated salivary flow rate
1. 45-50% from parotid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does salivary flow fluctuate during the day?

A 
Sleep
1. 40ml over 7 hours
Awake
1. 300ml over 16 hours (unstimulated)
2. 200ml over 54 minutes (stimulated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

State type of saliva secretion with each gland and the duct associated with it when applicable

A
  1. Parotid; serous saliva (Stenson’s duct)
  2. Submandibular; serous and mucous saliva (Wharton’s duct)
  3. Sublingual; mucous saliva (Bartholin’s duct)
  4. Minor; mucous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What radiographs are appropriate to study the salivary gland?

A

This is usually used to detect calculi (but not all calculi are radio opaque)

  1. Parotid; panoramic/oblique lateral + anterior-posterior view radiograph
  2. Submandibular; panoramic + lower occlusal view (true and oblique)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are indications and contraindications of sialography?

A

Indications;
1. To show structural abnormalities of the duct system
2. Atrophy of salivary acini (in case of Sjögren’s a characteristic ‘snowstorm’ appearance is seen)
Contraindications;
1. Presence of acute infection
2. Patient in severe pain
3. Calculus is known to be close to the duct (contract medium may further displace the calculus)
4. Suspected ‘mass’ lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 phases demonstrated by sialography?

A
  1. Preoperatively
  2. The filling phase
  3. The emptying phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is sialadenitis?

A

Sialadenitis is the term used to describe inflammation of salivary gland (most commonly the result of viral or bacterial* infection)
*bacterial sialadenitis is usually a secondary consequence of either localised/systemic cause of reduced salivary flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the types of symptomatic relief options for xerostomia?

A 
Intrinsic (increases gland activity)
1. Sugar free gum
2. Pilocarpine 
Extrinsic
1. Saliva substitutes
a) Mucin based
b) Carboxymethylcellulose based
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the most common candidal species involved in oral candidosis?

A

Candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define Sjögren’s syndrome?

A

Sjögren’s syndrome is an autoimmune disease of the exocrine glands that particularly involve the salivary and lacrimal glands

  1. Primary; dry eyes (xerophthalmia) and dry mouth not associated with a connective tissue disease
  2. Secondary; dry eyes and dry mouth associated with a connective tissue disease (most commonly rheumatoid arthritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are predisposing factors for oral candidosis?

A
  1. Physiological: old age, infancy, pregnancy
  2. Local tissue trauma: mucosal irritation, dental appliance, poor oral hygiene
  3. Antibiotic therapy: broad spectrum
  4. Corticosteroid therapy: topical, systemic or inhaler
  5. Malnutrition: haematinic deficiencies
  6. Immune defects: AIDS
  7. Endocrine disorders: diabetes mellitus, hypothyroidism, Addison’s disease (primary adrenal insufficiency)
  8. Malignancies: leukaemia
  9. Salivary gland hypofunction: irradiation, Sjögren’s syndrome, xerogenic drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Briefly describe how a swab is carried out

A

A swab (moistened with sterile saline if necessary) is wiped along the surface of the lesion and placed in a suitable transport medium. The sample should be sent promptly to the microbiology laboratory for culture and sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the classification of oral candidosis?

A
  1. Group 1 (primary oral candidosis)
    Acute: pseudomembranous, erythematous
    Chronic: pseudomembranous, erythematous, hyperplastic
    Candida-associated-lesion: denture stomatitis, angular cheilitis, median rhomboid glossitis
  2. Group 2 (secondary oral candidosis)
    Oral manifestation of systemic mucocutaneous candidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the appropriate laboratory diagnosis of oral candidosis

A
  1. Swab test
  2. Smear test
  3. Biopsy (especially for chronic hyperplastic candidosis)
  4. Oral rinse
  5. Haematological tests (full blood count, serum ferritin/vitamin B12/ folate and blood glucose level)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some of the common therapy for treatment of oral candidosis?

A
  1. Polyene anti fungal agents
    Pros
    a) Available in various forms (lozenges/creams/suspensions)
    b) Relatively free from side effects
    c) Resistance is uncommon
    Cons
    a) Distinctive taste
    b) Poor patient compliance
    Examples
    a) Nystatin
    b) Amphotericin B
  2. Azoles
    Pros
    a) Available as systemic treatment (valuable for systemic disease)
    b) Miconazole is both anti fungal and anti bacterial
    Cons
    a) Resistance is common (problem with immunocompromised patient)
    b) Unfavourable pharmacokinetic interaction with a number of drugs including warfarin, statins, ciclosporine (immunosuppressant)
  3. Chlorhexidane could also be prescribed as it is antibacterial and anticandidal (but it should not be used together with nyastatin due to pharmacokinetic interaction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are key features of acute/chronic pseudomembranous candidosis?

A
  1. Also known as thrush
  2. Common in HIV and indicate low immunity (immunocompromised patients are usually associated with chronic candidosis)
  3. Creamy soft patches that are readily wiped off leaving a raw bleeding base
  4. Smear shows gram positive hyphae
  5. Histology shows hyphae invading superficial epithelium with proliferative and inflammatory response
  6. Has various predisposing factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are key features of acute erythematous candidosis?

A
  1. Also known as acute atrophic candidosis
  2. Resembles thrush without the overlying pseudomembrane
  3. Only variant of candida with pain association
  4. Epithelium is thin and atrophic with candidal hyphae embedded superficially in the epithelium
  5. This form of candidosis is common with AIDS patient (immunocompromised) as well as patients undergoing prolonged antibiotic/steroid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are features of chronic hyperplastic candidosis?

A
  1. Also known as candidal leukoplakia
  2. The lesion appear as raised irregular white plaques which may be “speckled” or nodular in appearance
  3. The plaque unlike thrush cannot be scraped off
  4. Hyphae grows into full thickness of the epithelium
  5. It is considered a premalignant lesion and it is more likely to occur in patients who smoke
  6. Most commonly on the commissures of the mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are key features of denture stomatitis?

A
  1. Also known as chronic erythematous candidosis
  2. Candidal infection due to trauma to tissues (caused by dental appliance)
  3. Marked redness of palatal mucosa (directly related to area covered by appliance)*
  4. Rarely associated with pain
  5. Gram stained smears show candidal hyphae
    * Newton’s classification of Candida-associated denture stomatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are key features of angular cheilitis?

A
  1. Multi factorial condition with a number of local and systemic predisposing factors
  2. In most cases, deep folds at the angle of the mouth become traumatised as a result of continual wetting by saliva
  3. It could also be a result of underlying systemic condition
  4. Angular cheilitis of bacterial origin (and not candida) is treated with fusidic acid cream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are key features of median rhomboid glossitis?

A
  1. Abnormality in the midline of the dorsum of the tongue immediately in front of the circumvallate
  2. Appears as an area of depapillation (may be red/white/yellow)
  3. Lesions often associated with candida
  4. Patient should undergo blood test to exclude haematinic deficiency or diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How many types of herpes simplex virus are there and which part of the body are affected by each virus respective?

A
  1. HSV type 1: oral mucosa, pharynx and skin

2. HSV type 2: predominant genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are key features of chronic mucocutaneous candidosis?

A
  1. Candidosis of the oral cavity, skin and other structures (fingernails)
  2. Skin lesion may include widespread and disfiguring lesion of the face and scalp
  3. Can be familial CMC or diffuse CMC
  4. Due to mutation in one/two specific genes causing malfunctioning T cell
  5. Oral lesion initially resemble thrush > resemble chronic hyperplastic candidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does herpes simplex virus (type 1) manifest itself?

A
  1. Primary infection: primary herpetic gingivostomatitis

2. Recurrent infection: herpes labialis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the typical features of herpes labialis?

A
  1. Caused by the reactivation of herpes simplex virus
  2. Commonly known as cold sore
  3. Recurrence may be provoked by various factors including menstruation, strong sunshine, common cold etc
  4. Occurs in 3 stage:
    Stage 1; tingling/burning/itching sensation
    Stage 2; appearance of vesicles surrounded by a mildly erythematous area
    Stage 3; fluid-filled vesicles burst and form a scab
  5. Whole process takes about 10 days
  6. Aciclovir and penciclovir are best treatment options
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the typical features of primary herpetic gingivostomatitis?

A
  1. Transmitted by close contact
  2. Vesicles followed by ulcers affecting any part of the oral mucosa
  3. Two most favourite sites for vesicles are hard palate and dorsum of tongue
  4. Gingivitis is sometimes associated (usually in children)
  5. Lymphadenopathy (swelling of lymph nodes) and fever of variable severity
  6. Smears from vesicles show ballooning degeneration of viral-damaged cells
  7. Rising titre of antibodies to HSV confirms the diagnosis
  8. Aciclovir is the treatment of choice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does the varicella zoster virus manifests itself?

A
  1. Primary infection: chickenpox

2. Reactivation infection: herpes zoster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are typical features of herpes zoster (of trigeminal area)?

A
  1. Typically affects the elderly
  2. Pain precedes the rash (2-3 days)
  3. Facial rash accompanies the stomatitis
  4. Lesions localised to one side, within any distribution of the divisions of the trigeminal nerve
  5. Malaise can be severe
  6. Can be life threatening in HIV patients
  7. Rising titre of VZV-specific IG-M antibody confirms diagnosis
  8. Best treatment option is systemic aciclovir (800mg x 5 times a day x 7 days)
  9. Sometimes followed by post herpetic neuralgia (particularly in elderly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are groups of Coxsackie virus?

A
  1. Group A (affects oropharyngeal region)

2. Group B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the two infections caused by Group A Coxsackie virus?

A
  1. Hand, foot and mouth disease

2. Herpangina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are key features of hand, foot and mouth disease?

A
  1. Highly infectious and occurs as mini-epidemics
  2. School children are predominantly affected (occasionally spreading to parents and teachers)
  3. The oral lesions consists of small ulcers relatively few in number and distributed all over the oral mucosa
  4. Macular (round) rash with vesiculation on PALMAR surface of hand and PLANTAR surface of feet
  5. Symptoms resolve in a week
  6. No specific treatment is available or needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the types of HPV infections associated with cervical and oral cancers?

A
  1. HPV 16

2. HPV 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are key features of herpangina?

A
  1. Mild infection predominantly in children that occurs in mini-epidemics
  2. Patient complains of malaise, sore throat with some degree of muscle weakness and pain
  3. Small vesicular lesion appear in the posterior part of the mouth (soft palate)
  4. Lesions fade after 3-5 days
  5. No treatment is available or needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does HPV virus manifests itself?

A

It causes warty lesions on the skin and mucous membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the key features of AIDS?

A
  1. Caused by retrovirus HIV 1
  2. Transmitted sexually, by intravenous drug abuse, blood and blood products
  3. Due to infection and consequent inactivation of CD-4 expressing cells (T helper cell) leading to functional disabling of the host’s immune system
  4. Deaths are mainly due to opportunistic infection
  5. Triple therapy is the most effective choice of treatment (protease inhibitor + nucleoside reverse transcriptase inhibitor + non nucleoside reverse transcriptase inhibitors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the two types of warts and where are they commonly seen?

A

Common wart (verruca vulgaris)
1. Skin and oral mucosa (due to auto inoculation by chewing warts on hands)
2. White cauliflower like lesion (indistinguishable from squamous cell papilloma)
Venereal warts (condyloma acuminatum)
1. Also known as genital warts
2. May occur in the mouth as a result of orogenital sexual contact
3. They appear as soft, pink papillary lesion particularly on the soft palate and tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the common oral lesion associated with HIV infection?

A
  1. Fungal: Thrush and other forms of candidosis
  2. Viral: Herpes simplex, varicella zoster, hairy leukoplakia (EB virus)
  3. Bacterial: HIV-associated gingivitis and periodontitis
  4. Tumours: Kaposi’s sarcoma, lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the causes of pulpitis?

A
  1. Dental caries
  2. Traumatic exposure of the pulp
  3. Fracture of a crown or cusp
  4. Cracked tooth syndrome
  5. Thermal or chemical irritation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are key features of reversible pulpitis?

A
  1. Transient and short duration of pain that resolves after stimulus is removed
  2. Occurs in response to hot, cold and sweet food
  3. Pain is described as short and sharp
  4. Progresses to irreversible pulpitis is left untreated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Define pulpitis

A

Inflammation of the dental pulp tissue due to bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why does pulpitis cause pain?

A
  1. Due to pressure on the irritated nerve endings by inflammatory infiltrate within rigid pulp chamber
  2. Due to release of pain-producing substances from damaged tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are key feature of irreversible pulpitis?

A
  1. Dull, aching, pulsing/throbbing pain
  2. Occurs spontaneously often at night (affects sleep)
  3. Occurs in response to thermal stimuli
  4. Pain persists after removal of stimulus
  5. Not affected (or very limited effect) by analgesics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When does acute pulpitis progresses to chronic pulpitis?

A
  1. Acute pulpitis: reversible pulpitis > irreversible pulpitis
  2. Chronic pulpitis: pulpal death > periapical periodontitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why is pulpal pain poorly localised?

A

The pulps of individual teeth are not precisely represented on the sensory cortex. Thus it may be felt in any of teeth of the upper/lower jaw of the affected site*
*rarely the pain may be referred to a more distant site such as the ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Compare and contrast periodontal and periapical abscess

A

Periapical Abscess
1. Manifestation of untreated apical periodontitis (due to bacteria and pulpal breakdown products leaving the canal and causing inflammation of the periodontal ligament)
2. Severe pain that disturbs sleep
3. Associated with intra oral and facial swelling
4. Tooth non vital and severely tender to percussion
Periodontal abscess
1. Manifestation of acute infection of the periodontal pocket
2. Gingival tenderness > throbbing pain
3. Tooth affected is vital and tender to percussion (not severe)
4. Overlying gingiva is red and swollen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are key features of psychogenic (atypical) facial pain?

A
  1. Women of middle age or older are mainly affected
  2. Absence of organic signs and triggering factors
  3. Pain often poorly localised
  4. Description of pain may be bizarre
  5. Delusional symptoms often associated
  6. Lack of response to analgesics
  7. Unchanging pain persisting for many years
  8. Sometime with good response to anti depressive treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How is an abscess formed?

A
  1. Bacteria causes tissue necrosis
  2. Pus forms by the action of neutrophil proteolytic enzymes
  3. The process is localised by granulation tissue forming the abscess wall*
    * surrounding tissues may become swollen by diffusion of inflammatory exudate into them (oedema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does fascial space infection differ from an abscess?

A

In fascial space infections (a form of cellulitis):

  1. Fasciae covering muscle bundles are normally in close apposition
  2. If these fascias are forced apart, avascular spaces are created
  3. If localisation of bacterial fails, inflammatory exudate open up fascial space, carrying bacteria with it into the tissue planes
  4. Unlike oedema the exudate in cellulitis form vehicle for spread of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the main types of deep fascial space infection?

A
  1. Sublingual
  2. Submandibular (separated by mylohyoid; submaxillary + sublingual)
  3. Parapharyngeal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the clinical features of fascial space infection/ cellutis?

A
  1. Diffuse swelling: tense and tender (board-like tenderness)
  2. Pain: limit opening of mouth and cause dysphagia (swallowing difficulty)
  3. Fever
  4. Malaise
  5. Overlying skin is taut and shiny
  6. Swollen regional lymph nodes
  7. Severe systemic upset associated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the key features of Ludwig’s Angina?

A
  1. Severe form of cellulitis usually arising from lower second or third molars
  2. Involves submandibular and sublingual spaces (bilaterally) > lateral pharyngeal and pterygoid spaces
  3. Painful swelling of upper part of neck and floor of mouth on both sides
  4. Tongue may be pushed up the soft palate or oedema of the glottis may occur
  5. Causes dysphagia and asphyxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the key requirements for management of Ludwig’s Angina

A
  1. Immediate admission to hospital
  2. Procurement of a sample for culture and sensitivity testing
  3. Aggressive antibiotic treatment
  4. Securing airway with tracheostomy if necessary
  5. Drainage of swelling to reduce pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are key features of atypical odontalgia?

A
  1. Pain is often localised to one tooth or a row of teeth
  2. Affected tooth/teeth are said to ache or exquisitely sensitive to heat, cold or pressure
  3. Treatment of dental disease has no effect and if extracted symptom moves to an adjacent tooth
  4. Psychiatric assessment is needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the two sources of TMJ pain?

A
  1. Muscles, joint structures and other associated tissue as a result of abnormal physical activity within the joint
  2. Pathological changes in the joint itself (may be associated with systemic abnormality)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the four key aspects in investigating the stomatognathic system?

A

Pain:
1. Within the joint or from the muscles of mastication
2. Constant with acute exacerbation (usually associated with radiation of pain from joint)
3. May occur in the morning or during the evening
4. Muscular pain may cause headache
Joint sounds
1. Represents the movement of one component of the joint over the others
2. Can mean that the disc is slipping out of place or malfunctioning
3. Presence of a click on its own does not indicate a problem
Restriction of opening
1. Some report difficulty in wide opening
2. Others may have problems applying pressure or closing mouth
3. The inability to open mouth widely due to reflex muscular spasm of the masticatory muscles is known as trismus (temporary)
4. Patient often complains that their jaw ‘locks’. This is due to the disc being squashed and bunched up anteriorly preventing further opening
Swelling
1. Patients occasionally complain of swelling over the maxilla/parotid
2. Tenderness is also often associated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the normal amount of mandibular opening?

A

Inter-incisal opening of approximately 35-45mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the muscles that should be palpated in association with TMJ dysfunction?

A
  1. Masseter

2. Temporalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are other terms used to describe temporomandibular pain dysfunction syndrome?

A
  1. Myofacial pain dysfunction
  2. Facial arthromyalgia
  3. Facial pain dysfunction
  4. Masticatory muscle disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the signs and symptoms associated with temporomandibular pain dysfunction syndrome?

A
  1. Pre auricular pain that may radiate to other sites
  2. Tenderness of the joint on palpating
  3. Limited jaw movement or deviation of mandible on opening/closing
  4. Tenderness of masticatory muscles on palpation
  5. Joint sound (clicking/crepitus)
  6. Headache
71
Q

Which parts of the body are affected by giant cell arteritis?

A

Giant cell arteritis can affect many parts of the body but the head is often involved:

  1. Temporal artery: temporal/cranial arteritis
  2. Other parts of body: polymyalgia rheumatica
72
Q

Define giant cell arteritis

A

Inflammatory condition that typically affects the walls of medium-sized arteries. The lumen of the vessels becomes compromised and as a consequence ischaemia of the tissues supplied by the artery may occur

73
Q

What are key features of temporal arteritis?

A
  1. Primarily affecting elderly people (~70 years old)
  2. Pain is localised to the temporal and frontal region (area supplied by superficial temporal artery)
  3. Pain is described at severe, throbbing ache
  4. Sudden onset pain/headache that is initiated/exacerbated by eating (due to ischaemia of the muscles of mastication) and as a consequence weight loss may ensue
  5. Blindness is a recognised complication (involvement of retinal artery > ischaemia of optic nerve)
  6. Abnormally high erythrocyte sendiment rate (ESR) of over 100mm in 1 hour
  7. Biopsy of affected vessel may show typical giant-cell inflammatory process
  8. Treat with high dose systemic steroid (60mg prednisolene)
74
Q

What is trigeminal neuralgia?

A

Sudden, usually unilateral, severe, brief, stabbing, recurrent pains in the distribution of one or more branches of the 5th cranial nerve

75
Q

What are causes of of trigeminal neuralgia?

A
  1. Vascular abnormality that causes compression of the trigeminal root (adjacent to pons in posterior cranial fossa) which results in the areas of demyelination and abnormal nerve conduction
  2. Posterior fossa tumour
76
Q

What are the key features of trigeminal neuralgia?

A
  1. The peak onset is in the 5th to 7th decade (symptoms usually occur 4th decade)
  2. Pain confined to the distribution of one or more divisions of the trigeminal nerve (almost always unilateral)
  3. Provoking factors include eating, talking, shaving, washing face with presence of trigger zones
  4. The pain is of great intensity, described as sharp and stabbing and lasts only a few seconds
  5. This transient attack may be repeated in matter of minutes or hours but usually pain free during sleep
  6. Diagnosed principally from pain history (after excluding dental causes)
77
Q

What is the medical management of trigeminal neuralgia?

A
  1. Primarily with the use of anticonvulsant
  2. Carbamazepine* is currently the drug of choice
  3. The initial dose is started at 100mg x2 daily
  4. The dose is gradually increased by 100mg each day until pain is controlled
  5. A maximum dose of 800-1000mg should not be exceeded
    * carbamazepine should be used with caution;
  6. Should not be prescribed with Warfarin
  7. Drowsiness, dizziness, confusion, nausea and skin rash are all side effects
  8. Haematological effects have also been linked
  9. Thus full blood count, liver function test and electrolytes should be monitored a) prior to therapy b) at 1 month c) at 3 months
78
Q

What are key features of glossopharyngeal neuralgia?

A
  1. Similar to trigeminal neuralgia in nature but involves the glossopharyngeal nerve (the occurrence is also much less common)
  2. The pain is also of the same nature (paroxysmal, sharp, lanceting pain) that affects ONE side of the throat and base of tongue
  3. It is usually triggered by swallowing and chewing and there may be trigger zones
  4. Glossopharyngeal neuralgia may be secondary to tumours of the throat, posterior cranial fossa or jugular foramen
  5. Treatment is also the same as trigeminal neuralgia (carbamazepine)
79
Q

Define oral dysaethesia

A

Term used to denote disturbances of the oral sensation which includes condition like burning mouth syndrome

80
Q

What are key feature of pre/post herpetic neuralgia?

A

Pre herpetic neuralgia
1. Severe burning pain occurring along the nerve involved up to 2 days before appearance of vesicles
2. This pain usually subsides within weeks for most patients
Post herpetic neuralgia
1. In elderly patients (~ 60 years old) neuralgia pain persists for months even years after reactivation of varicella zoster virus (in the form of herpes zoster)
2. The pain has an intense burning component and may be accompanied by stabbing sensation
3. The distribution of pain follows that of the original infection
4. The neuralgia tends to be more persistent rather than paroxysmal pain (spontaneous)
5. There is no treatment for postherpetic pain (no responsive to drugs of any type). Prophylaxis offers the best hope in preventing postherpetic neuralgia (systemic antiviral treatment for herpes zoster)

81
Q

What are the key features of burning mouth syndrome?

A
  1. Middle aged or older women are mainly affected
  2. No visible abnormality of evidence of organic disease
  3. No haematological abnormality (full blood count, serum b12, red blood cell folate, serum ferritin, blood glucose)
  4. Pain is typically described as burning
  5. Persisting and unremitting soreness without aggravating or relieving factors (often for months or years of duration)
  6. No response to analgesics
  7. Bizarre pattern of pain radiation (inconsistent with neurological or vascular anatomy)
  8. Associated depression, anxiety or stressful life situation (also related to cancer phobia)
  9. Some patients respond with reassurance, others may need antidepressant medication
82
Q

What are key features of migraine?

A
  1. Intense throbbing, pulsating and continuous headache (usually unilateral temporal, occipital or frontal region)
  2. Each attack may last for several hours or even days
  3. Patients may experience ‘aura’ whereby the headache is preceded by neurological symptoms and deficits (visual/sensory/motor) which lasts around 15 minutes
  4. Some patients recognise precipitating factors (stress/food)
  5. Aetiology has been attributed to instability of cranial arteries
  6. Treat with simple analgesic, anti emetic (drug against nausea) or NSAID (aspirin, ibuprofen)
  7. Migraine prophylaxis is recommended for patients with 2 or more severe attacks each month: beta-blockers (propranolol), 5-HT1 antagonist (Pizotifen)
83
Q

What are key features of cluster headaches?

A
  1. Episodic severe pain of 30-180 mins that interrupts with sleep as it often occurs at night
  2. Male to female ratio is 9:1 (usually >20 years old)
  3. Pain is usually unilateral in the orbital region
  4. Aetiology is thought to be due to vascular changes at the base of skull
  5. Attacks may be precipitated by alcohol or vasodilator
  6. Obvious vascular changes in the affected site is seen (watery eyes, nasal congestion, red cheeks)
  7. Patient experience pain over a short period following by long periods of remission (where they are pain free for months/years)
  8. Simple analgesics, anti migraine drugs and subcutaneous injections of Sumatriptan
84
Q

What is leukodema?

A
  1. Leukodema is a bilateral diffuse translucent greyish thickening, particularly of the buccal mucosa
  2. It is a variation of normal mucosa present in 90% of blacks and a variable number of whites
  3. Treatment is unnecessary but reassurance may be required
85
Q

What are key features of frictional keratosis?

A
  1. Dense and white patches with rough surface
  2. Thick hyperkeratosis with no dysplasia
  3. Removal of the irritant causes patch to quickly disappear and there would be no need of biopsy unless patch persists
  4. Frictional keratosis is completely benign
87
Q

What are Fordyce’s granules?

A
  1. Sebaceous glands that grow in size with age and appear in the oral mucosa as soft, symmetrically distributed creamy spots a few millimetres in diameter (particularly in older people)
  2. The buccal mucosa is the main site but sometimes the lips are involved
  3. Biopsy would show normal sebaceous gland with two or three lobules
87
Q

What are key features of hairy leukoplakia?

A
  1. Vertically corrugated, shaggy plaque usually painless and most frequently affects the lateral borders of the tongue
  2. Diagnosis by biopsy where histologically, koilocyte-like cells are present (vacuolated and ballooned prickle cells with shrunken and dark nuclei surrounded by a clear halo)
  3. Epstein-Barr virus antigens detectable in epithelial cell nuclei by in-situ hybridisation
  4. Indicates advanced immunodeficiency and poor prognosis but not premalignant
88
Q

What are key features of stomatitis nicotina?

A
  1. Also known as pipe smoker’s keratosis
  2. The palate is affected but any part protected by denture is spared (changes here will only be seen on the soft palate)
  3. The lesion has two components;
    a) Hyperkeratosis
    b) Inflammatory swelling of minor mucous gland
  4. Typically appears as white thickening of the palatal mucosa with small umbilicated swellings with red centres
  5. Responds rapidly to abstinence from pipe smoking
  6. Pipe smoking does raise the risk for oral cancer but not in the keratotic area
89
Q

What are the key features of oral lichen planus?

A
  1. More commonly in females (65% of patients are female)
  2. Disease of the middle aged and elderly (patients are usually over 40 years)
  3. Oral lesions are usually bilateral and symmetrical
  4. Buccal mucosa is the most common site while the dorsum of tongue, palate, gingiva and lips can be affected
  5. Lesions can occur in combination or isolation (with reference to the different types of lesion)
  6. Cutaneous lesions are occasionally associated
  7. Histologically, subepithelial band of T lymphocytes can be seen
90
Q

What are key features of white sponge neavus?

A
  1. Developmental anomaly inherited as an autosomal dominant trait
  2. The affected mucosa is white, soft and irregularly thickened (including areas that are not subjected to friction)
  3. The white areas lack borders and can involve the whole mucosa
  4. There are no dysplasia and inflammatory cells in the lamina propria (corium)
  5. Histologically there is epithelial hyperplasia (increased cell proliferation but regulated) with a basket weave appearance
91
Q

Which types of lichen planus are often associated with pain?

A
  1. Erosive

2. Atrophic

92
Q

List the different clinical types of lichen planus

A
  1. Reticular: lace-like striae
  2. Atrophic: diffuse red lesion resembling erythroplakia
  3. Plaque-like: white plaques resembling leukoplakia
  4. Papular: small white papules that may coalesce
  5. Erosive: extensive areas of shallow ulceration
  6. Bullous: subepithelial bullae
  7. Desquamative gingivitis
93
Q

What are the key features of skin lichen planus?

A
  1. Dusky pink papules that is most commonly found on the flexor surface of wrists (also abdomen, lumbar, ankles, shins and genital skin)
  2. Fine white striation overlie the papules and are known as Wickham’s striae
  3. Some patients experience ridging and grooving of fingernails
95
Q

What is the widely accepted aetiology of lichen planus?

A

Cell-mediated immune response to an external antigen or internal antigen in the epithelial cells

96
Q

List the features that are suggests a lichenoid reaction

A
  1. Onset associated with starting a drug
  2. Unilateral lesions or unusual distribution
  3. Unusual severity
  4. Widespread skin lesion
  5. Localised lesion in contact with restoration
96
Q

What are the systemic diseases associated with lichen planus?

A
  1. Chronic liver disease
  2. Hepatitis C infection
  3. Graft vs Host disease
97
Q

What are some of the substances capable of causing lichenoid reaction?

A
  1. Non steroidal anti inflammatory drug
  2. ACE inhibitors
  3. Oral hypoglycemics
  4. Diuretics
  5. Anti malarial
  6. Colloidal gold (treatment of rheumatoid arthritis)
  7. Mercury salts from amalgam restorations
  8. Allopurinol (treats gout)
99
Q

What are the investigations that should be carried out for lichen planus?

A
  1. Swabs and smear to rule out candida
  2. Incisional biopsy of site involved
  3. Blood test
100
Q

What are the principles of management for lichen planus?

A
  1. Topical corticosteroid: betamethasone mouthwash, hydrocortisone pellets
  2. Systemic steroids for severe cases
  3. Antiseptic mouthwash: chlorhexidane
  4. Analgesic mouthwash: lignocaine rinse
101
Q

What is the long term management of lichen planus?

A

Long term review as a small proportion of oral lichen planus undergo malignant change

101
Q

What are the clinical features of leukoplakia?

A

Homogenous
1. Flat, uniform, predominantly white plaques
2. May show shallow crack/fissures
Non homogenous*
1. Irregular, nodular, thickened surface
2. Often speckled with areas of erythroplakia
*non homogenous lesions have worse malignant prognosis

102
Q

Define leukoplakia

A

White lesion of the oral mucosa that cannot be characterise clinically or pathologically as any other definable lesion

104
Q

Define erythroplakia

A

Bright-red velvety plaque on the oral mucosa which cannot be categorised clinically or pathologically as being due to another condition

105
Q

What are the aetiological factors associated with oral leukoplakia?

A
  1. Tobacco: either smoked or chewed
  2. Betel nut and lime (associated with tobacco chewing)
  3. Candida: found in candidal leukoplakia and idiopathic leukoplakia
  4. Alcohol: no clear evidence
  5. Viruses: HPV 16 and 18 are associated with carcinoma in the cervix
  6. Epithelial atrophy: tendency of leukoplakia to develop in atrophic epithelium
  7. Tumour supressor gene: seen in leukoplakia showing dysplasia
105
Q

What are key features of speckled leukoplakia?

A
  1. Lesions consisting of white flecks or dive nodules on an atrophic erythematous base
  2. Regarding as combination of erythoplasia and leukoplakia
  3. Also more frequently show dysplasia than lesions with homogenous white surface
106
Q

What are key features of erythroplasia?

A
  1. Also known as erythroplakia
  2. They usually don’t form plaque but rather flat and depressed below the level of surrounding mucosa
  3. Uncommon in the mouth but carries the highest risk of malignant transformation (lesions are often already malignant on first biopsy)
  4. Usually show severe epithelial dysplasia
107
Q

List histological features of epithelial dysplasia

A
  1. Drop-shaped rete ridges
  2. Nuclear hyperchromatism
  3. Nuclear pleomorphism and altered nuclear/cytoplasmic ratio
  4. Excess mitotic activity
  5. Loss of polarity of cells
  6. Deep cell keratinisation
  7. Disordered or loss of differentiation
  8. Loss of intracellular adherence
108
Q

Where are key features of idiopathic leukoplakia?

A
  1. Tough, adherent and typically form plaque whose surfaces are slightly raised above the surrounding mucosa
  2. Can appear as white patches, nodular or verrucous
  3. Most common sites are posterior buccal mucosa, retromolar region, floor or mouth and tongue
  4. Histologically can vary from hyperkeratosis without epithelial dysplasia to dysplasia to carcinoma in situ
109
Q

What are the key features of hereditary gingival fibromatosis?

A
  1. The most common type is autosomal dominant (associated also with mental retardation)
  2. Gingival enlargement may precede eruption of teeth or may not develop until later in childhood (during transition phase between deciduous to permanent dentition)
  3. The gingivae may be grossly enlarged as to completely bury the teeth
  4. The gingivae are pale, firm and smooth (or coarsely stippled)
  5. Histologically the gingival tissues consist of thick bundles of collagenous connective tissue with little or no inflammatory exudate
  6. Gingivectomy is treatment of choice but should be delayed until puberty (where rate of tissue growth slows down)
110
Q

What is a hamartoma?

A

Localised non progressive tissue abnormality resulting from a defect in development. When present in the skin or mucous membrane, the term naevus is used

111
Q

What are two types of dental abscess?

A
  1. Periodontal abscess

2. Periapical abscess

112
Q

What are key features of hemangioma?

A
  1. Development abnormality (hamartoma) in the vascular component of the mucosa
  2. Also known as vascular naevae which a relatively common lesion of the oral mucosa
  3. Depending on degree of dilation, they may appear as fine network of capillaries or a more pronounced nodular structure filled with venous blood (thus a dark blue colour)
  4. The lesions blanch upon pressure which differentiates them from melanomas
  5. It it seen most commonly on the tongue and lips
  6. Excision of mucosal haemangioma should be avoided unless trauma causes repeated episodes of bleeding (cryosurgery may allow it to be removed without excessive bleeding)
113
Q

What are key features of an abscess?

A
  1. Results from acute infection of a periodontal pocket
  2. Affected tooth is extruded, mobile and tender to percussion
  3. Associated with localised intra oral swelling and pus exudation from affected tooth
  4. Radiographic varies based on periodontal or periapical abscess:
    a) Periodontal: vertical or horizontal bones loss
    b) Periapical: ranges from widening of apical PDL to obvious radiolucency
  5. Management is by drainage of pus and antibiotics is prescribed IF there is systemic involvement (fever, malaise etc)
115
Q

What is an epulis?

A
  1. Soft tissue swelling of the gingival margin
  2. More specifically it is used to describe a range of hyperplastic inflammatory lesion arising from periodontal tissues (exaggerated inflammatory response of the periodontium)
  3. More common in females than men
  4. Usually occur anterior to molar teeth
116
Q

What are types of epulides?

A
  1. Pyogenic granuloma
  2. Fibrous epulis
  3. Pregnancy epulis
  4. Giant cell epulis
117
Q

What are features of fibrous epulis?

A
  1. Pedunculated swelling in the gingivae
  2. Consists of heavily fibrosed granulation tissue
  3. It’s content of collagen fibres gives it a firm, rubbery texture and its colour is usually pale pink
  4. However following a trauma or infection, acute inflammatory changes may occur and the epulis may become red and sore
  5. Most frequently formed at the gingival margin or in relation to denture (denture granuloma)
  6. Over time, focal mineralisation and/or bone formation can occur
118
Q

What are features of pyogenic granuloma?

A
  1. Presents clinically as a reddish-purple swelling on the gingivae
  2. Vascular epulides consisting of dilated blood vessels
  3. Histologically identical to pregnancy epulides (only patient factor distinguishes the both)
  4. Remains vascular and immature
  5. Much redder in colour that fibrous epulis proper
  6. Has the tendency to bleed easily due to its high vascular content
119
Q

What are key features of giant cell epulis?

A
  1. Lesion in which granulation tissue is osteogenic in nature
  2. In its immature form the swelling is rounded, soft and typically maroon or purplish
  3. Histologically, there are multinucleated giant cells dispersed in a vascular stroma
  4. With maturity the lesion becomes less vascular and more fibrosed and include areas of bone formation
  5. Usually found on the gingival margin between teeth anterior to permanent molars
120
Q

How are epulides managed?

A
  1. Local excision is treatment of choice
  2. Initial removal should include all affected tissues to prevent recurrence
  3. Clinical diagnosis should be confirmed with a histological examination
  4. With regards to giant cell epulis, blood test for plasma calcium, phosphorus and alkaline phosphotase should be carried out to exclude hyperparathyroidism
121
Q

What are key features of fibroepithelial polyp?

A
  1. Scar tissue produced as a response to trauma due to repeated irritation to labial or buccal mucosa along the occlusal plane of teeth (often caused by a bite)
  2. Usually seen in adults but without sex differentiation
  3. The lesion appears as a pedunculated swelling similar in structure to fibrous epulis
  4. The lesion is pink in colour and the texture varies form soft to rubbery
  5. Treatment is by excision (conservative) as it is simply an exaggerated mass of scar tissue
122
Q

Define cyst

A

A pathological cavity having fluid or semi-fluid contents which has not been created by the accumulation of pus

122
Q

Describe the origins of odontogenic cyst

A

Derived from epithelial residues of the tooth forming organ. The main cysts derived from each residue:

  1. Dental lamina rests/glands of Serres
    a) Odontogenic keratocytes
  2. Reduced enamel epithelium
    a) Dentigerous cyst
    b) Paradental cyst
  3. Rests of Malassez
    a) Radicular cyst
123
Q

What are the two main groups of cyst?

A

They are divided according to the origin of the lining epithelium:

  1. Odontogenic cyst: the epithelial lining is derived from the epithelial residues of a tooth forming organ. They are subdivided into:
    a) Developmental
    b) Inflammatory types
  2. Non odontogenic cyst: the epithelial lining is derived from sources other than the tooth forming organ
125
Q

What are the 3 types of radicular cyst (periapical cyst)?

A
  1. Apical
  2. Lateral
  3. Residual
    * this depends on the anatomical relationship of the cyst to the root of the tooth
126
Q

What are key features of apical radicular cyst?

A
  1. The most common cystic lesion in the jaws (also account for 75% of all radicular cysts)
  2. Always associated with the apices of non vital teeth
  3. Most common between 20-60 years of age
  4. When small they are symptomless and usually discovered during a routine radiographic examination
  5. On a radiograph it presents as a round or ovoid radiolucency at the root apex (indistinguishable from a periapical granuloma)
  6. Enlargement of the cyst leads to bone expansion
  7. The maxilla is affected more that x3 frequently compared to the mandible
  8. Arises by epithelial proliferation in an apical granuloma
126
Q

What are the main factors in the pathogenesis of cyst formation?

A
  1. Proliferation of epithelial lining and fibrous capsule
  2. Hydrostatic pressure of cyst fluid
  3. Resorption of surrounding bone
127
Q

Describe the process of a radicular cyst enlargement

A
  1. The cyst enlarges and causes bone resorption centrally
  2. Increments of subperiosteal bone are laid down to maintain the integrity of the cortex
  3. This produces a bony-hard expansion of the alveolar bone
  4. However, rate of expansion tends to outstrip the rate of subperiosteal deposition
  5. This leads to progressive thinning of the cortex
  6. Clinically this presents as ‘egg shell crackling’ sensation when palpated with pressure
  7. Eventually the cyst may perforate the cortex and presents as a bluish, fluctuant, submucoal swelling
128
Q

What is residual radicular cyst?

A

Radicular cyst that has remained in the jaw and failed to resolve following extraction of the involved tooth

129
Q

Describe the treatment a radicular cyst

A

Ennucleation is the method used:

  1. The affected tooth can either be extracted or root filled
  2. A mucoperiosteal flap over the cyst is raised
  3. A window is opened in the bone to give adequate access
  4. The cysts is carefully separated from its bony wall
  5. Edges of the bone cavity are smoothed, bleeding controlled and cavity is irrigated to remove debris
  6. Mucoperiosteal flap is replaced and sutured in place
130
Q

What is a dentigerous cyst?

A

A cyst surrounding the crown of an unerrupted tooth and is a dilation of the follicle

131
Q

What is a paradental cyst?

A
  1. Results from inflammation around a partially erupted teeth (particularly mandibular third molar)
  2. Affected tooth is vital but typically shows pericoronitis
133
Q

What are the key features of a dentigerous cyst?

A
  1. The cyst is attached to the amelocemental junction of the tooth and prevents its eruption
  2. Twice more common in males than in females
  3. Most frequently involve impacted or late-erupting teeth (canine and third molars)
  4. Lined by thin, non keratinising squamous epithelium
  5. Radiographically presents as a well defined unilocular, radiolucency associated to the crown of the tooth
  6. The tooth is often displaced a considerable distance
  7. Responds to enucleation or marsupialisation and do not recur after treatment
134
Q

What are key features of eruption cyst?

A
  1. Affect children and involve teeth having no predecessor (deciduous teeth or permanent molars)
  2. A superficial dentigerous cyst
  3. Lies superficially in the gingiva overlying the unerupted tooth and appears as a soft, rounded, bluish swelling
  4. Cyst may be removed to allow teeth to erupt or burst spontaneously
134
Q

What is marsupialisation?

A

A surgical technique of removing cyst whereby the lining of the cyst sutured to the mucous membrane at the margins of the opening

135
Q

What are key features of odontogenic keratocyst?

A
  1. Form intraosseously, most frequently in the posterior alveolar ridge or angle of mandible
  2. May grow around a tooth
  3. Symptomless until the bone is expanded or the cyst becomes infected
  4. The expansion of the jaw is much less other cysts (can reach large sizes without causing gross bony expansion)
  5. Sometimes multilocular (multiple compartment) radiographically
  6. There is a tendency to recur after enucleation
  7. Does not respond to marsupialisation
  8. May be part of basal cell neavus syndrome
  9. Histologically lined by stratified squamous epithelium and contains keratinous debris which sometimes can be extruded from the cyst roof
136
Q

What are features of nasopalatine duct cyst?

A
  1. The most common non odontogenic cyst
  2. Often a symptomatic and discovered by chance on radiographs
  3. Developmental lesion arising from epithelial remnants of nasopalatine duct (connecting the oral and nasal cavities in embryo)
  4. Do not recur after enucleation
137
Q

What is the most common cancer of the mouth?

A

Squamous cell carcinoma

138
Q

What are features of extravasation mucoceles?

A
  1. Most commonly found in the lower lip, followed by cheek and floor of mouth (extremely uncommon in the upper lip)
  2. Clinically presents as a bluish or translucent submucosal swelling
  3. Caused by damage to the duct of the mucous gland (trauma to the lip) > extravasation of saliva > saliva leaking into surrounding tissues causes mild inflammation > saliva eventually pools up to form mucocele with connective tissue lining
139
Q

List the possible etiological factor for oral cancer

A
  1. Possible carcinogens
    a) Tobacco
    b) Alcohol
    c) Areca/betel nut
  2. Sunlight (lip only)
  3. Infections
    a) Syphilis
    b) Candidosis
    c) Viruses
  4. Mucosal disease
    a) Oral epithelial dysplasia
    b) Lichen planus
    c) Oral submucous fibrosis
  5. Genetic disorder (rare)
    a) Fanconi’s anaemia
    b) Dyskeratosis congenita
140
Q

What is the most common site for oral cancer?

A
  1. Lower lip is most frequent site overall
  2. Within the mouth, the common sites are as follows:
    a) Lateral borders of the tongue (most common)
    b) Retromolar pad area
    c) Lingual aspect of alveolar margin
    d) Floor of the mouth
141
Q

What are clinical features suggestive of oral carcinoma?

A
  1. Persistent, unexplained ulceration (lasting for more than 10 days)
  2. Induration (thickening and hardening of tissues)
  3. Proliferative growth
  4. Changes in texture and colour
  5. Fixation to underlying tissues
  6. Sudden loosening of teeth (replacement of periodontal ligament with tumour)
  7. Lymph node involvement
  8. Pain (of the a late feature)
142
Q

What are potentially malignant disorders that can progress to squamous cell carcinoma?

A
  1. Erythroplakia
  2. Lichen planus
  3. Speckled leukoplakia
  4. Submucous fibrosis
143
Q

What is the treatment of oral cancer?

A
  1. Surgery (with or without neck dissection) and reconstruction
  2. Surgery, reconstruction and radiotherapy (in case of metastasis)
  3. Clearance of infection foci before radiotherapy
  4. Life long need for intense dental care
144
Q

What is torus palatinus?

A

Bony protrusion of the palate

146
Q

Define an ulcer

A

Localised defect of the surface of the oral mucosa in which covering epithelium is destroyed, leaving an inflamed area of exposed connective tissue

147
Q

What are the causes of oral ulceration?

A
  1. Infective: bacterial, viral or fungal
  2. Traumatic: mechanical, chemical, thermal, fictitious injury, radiation and eosinophilic ulcer (traumatic granuloma)
  3. Idiopathic: recurrent aphthous stomatitis
  4. Associated with systemic disease: haematological disease, GI tract disease, Behçet’s disease and HIV infection
  5. Associated with dermatological disease: lichen planus, vesiculobullous disease and chronic discoid lupus erythematous
  6. Neoplastic: squamous cell carcinoma and other malignant neoplasms
148
Q

List the 3 criteria of traumatic ulcers that should be fulfilled

A
  1. A cause of trauma must be identified
  2. The cause must fit the site, size and shape of the ulcer
  3. On removal the ulcer must show signs of healing within 10 days
    * a traumatic ulcer shows histological features of chronic non specific inflammation and they frequently develop a keratotic halo during their healing phase
148
Q

Where is acute thermal trauma from taking hot food and drinks most commonly seen?

A

The palate (although it can occur in any part of the mucosa)

149
Q

What are common chemical causes of a traumatic ulceration?

A
  1. Antiseptic mouthwash that has not been diluted properly (or other caustic agents used in the dental practice)
  2. Aspirin misuse by patients as a local analgesic for tooth ache relief
    a) The caustic action of aspirin is dose and time related
    b) Reaction may vary from oedema to necrosis of the epithelium
    c) The necrotic epithelium presents as soggy white plaques which slough off to leave areas of ulceration
150
Q

What are features of factitious ulcers?

A
  1. They are self inflicted and may be manifestation of stress, anxiety or more severe emotional disturbances
  2. They appearance vary considerably based on how they are inflicted
  3. Common causes are biting/chewing of lips, cheeks or tongue and damage to the gingivae from sharp finger nails
152
Q

How does radiotherapy causes ulcers?

A

Immediate damage
1. Direct effects of radiation on the cells
2. These effects include
a) Erythema (redness of mucous membrane)
b) Radiation mucositis
c) Ulceration
Delayed
1. Epithelial atrophy and damage to underlying vascular bed
2. These effects render the mucosa susceptible to trauma and even minimal trauma can cause ulceration

153
Q

Distinguish ulcers and erosion

A
  1. Erosion refers to defect of the surface (of the oral mucosa) where there is incomplete loss of epithelial covering (more shallow)
  2. An ulcer exhibit complete loss of epithelium in the region of the lesion
153
Q

List the aetiological factors in recurrent aphthous stomatitis

A 
Aggravating factors:
1. Trauma
2. Emotional stress and other physiological factors
3. Bacterial and viral infection
4. Hormonal disturbances
5. Smoking cessation 
Real aetiological factors
1. Haematological and deficiency disorder (iron, folate and vitamin B12)
2. Gastrointestinal disease
3. Allergic disorder
4. Hereditary predisposition
154
Q

What are features suggestive of factitious oral lesion?

A
  1. Lack of correspondence to any recognisable disease
  2. Bizarre configuration with sharp outlines
  3. Usually in an otherwise healthy mouth
  4. Clinical features inconsistent with the history
  5. In areas accessible to the patient
155
Q

What are the 3 types of recurrent aphthous stomatitis?

A
  1. Major aphthous ulcers
  2. Minor aphthous ulcers
  3. Herpetiform apthae
    * the onset of RAS is frequently in childhood but peaks in adolescence or early adult life
156
Q

What are key features of minor apthous ulcerations?

A
  1. The most common type
  2. Non keratinised mucosa affected
  3. Ulcers are shallow, rounded, 5-7mm across with an erythematous margin and yellowish floor
  4. One or several ulcers may be present
  5. They heal without scarring within 10 days
157
Q

What are the key features of major apthous ulceration?

A
  1. Uncommon
  2. Ulcers frequently several centimetres across
  3. Sometimes mimic a malignant ulcer (crater like ulcers)
  4. Ulcers persist for several months (may take 4-6 weeks to heal)
  5. Masticatory mucosa such as dorsum of tongue or gingivae may be involved in addition to non keratinised surface
  6. Scarring may follow healing
158
Q

What are key features of herpetiform ulceration?

A
  1. Uncommon
  2. Characterised by multiple small pin-head sized ulcers (1-2mm)
  3. Occurs on non keratinised surface but particularly lateral margin/ventral of tongue and floor of mouth
  4. Dozens to hundreds ulcers may be present
  5. May coalesce to form irregular ulcers (which may cause scarring)
  6. Wide spread bright erythema around the ulcers
159
Q

How is Behçet’s syndrome linked to recurrent apthous stomatitis?

A

Behçet’s disease is characterised by recurrent apthous stomatitis and at least two of the following:

  1. Genital ulcers
  2. Eye lesion
  3. Skin lesion
  4. Rapid acute inflammation of skin in response to minor trauma
  5. Arthritis
160
Q

What is the main histopathlogy of recurrent apthous stomatitis?

A

Immune-mediated cytotoxic damage to the oral epithelium due to increased activity of T cell subpopulation.

161
Q

What is the link between recurrent apthous stomatitis and smoking?

A

This disease is one that is almost exclusively to non smokers. May also start when smoking is abandoned

162
Q

What are the investigations for patients with persistent recurrent apthous stomatitis?

A
  1. Haemoglobin and full blood count
  2. ESR/CRP
  3. Serum B12
  4. Red cell folate
  5. Anti endomysial autoantibodies and anti transtissueglutamase (TTG)
163
Q

What is the management of patients with recurrent apthous stomatitis?

A

Objective of treatment is only to relieve discomfort and reduce secondary infection

  1. Topical antiseptic: chlorhexidane gluconate mouthwash
  2. Topical analgesic: benzydamine hydrochloride mouthwash
  3. Topical corticosteroid: hydrocortisone hemisuccinate pellets
  4. Topical antibiotic: tetracycline mouthwash
165
Q

Distinguish between a vesicle and bulla

A

Both vesicles and bulla are collection of clear fluid within or just below the epithelium. However a bulla is a lesion that is greater than 5mm in diameter and lesion smaller than that is a vesicle

166
Q

What are the two major groups of vesiculobullous lesion?

A

The two groups are depending on their histological lesion

  1. Intraepithelial vesicles: lesion formed within the epithelium
    a) Acantholytic vesicles and bullae: the lesions are produced from breakdown of specialised intracellular attachments (desmosomes) between epithelial cells (Eg: pemphigus)
    b) Non acantholytic vesicles or bullae: the lesions are produced by death and rupture of groups of epithelial cells (Eg: viral infections of oral mucosa)
  2. Subepithelial vesicles: lesion formed between the epithelium and lamina propria (Eg: pemphigoid)
167
Q

What are the key features of pemphigus vulgaris?

A
  1. Uncommon autoimmune disease causing vesicles or bullae on skin and mucous membrane
  2. Females predominantly affected usually aged 40-60 years old
  3. Lesions often first in the mouth but spread widely on the skin (fatal if left untreated)
  4. Lesions consists of fragile vesicles or bullae which readily rulture forming crusted or weeping areas of irregular, ragged ulcer on the mucosa
  5. Nikolsky’s sign may be positive (gentle lateral pressure to the mucosa of involved area leads to formation of bulla)
  6. High incidence of condition among Jewish people
  7. Pemphigus vulgaris is the most common type of pemphigus
167
Q

What is the management of pemphigus vulgaris?

A

Diagnosis
1. Immunofluorescence microscopy to detect direct binding of autoantibodies to the intracellular area of epithelium
Treatment
1. Immunosuppressive treatment: 80-100mg/day of prednisolone plus azathioprine (to reduce effect of corticosteroid)

168
Q

Describe the immunopathology of pemphigus vulgaris

A
  1. The desmosomes is a junctional complex mediating cell-cell contact
  2. It compromises of intercellular attachment plaque and adhesion proteins
  3. Desmogleins are important transmembrane adhesion protein
  4. High titres of auto antibodies to desmoglein 1 and 3 are found in pemphigus involving skin and mucosa
  5. Breakdown of desmosomes lead of acantholysis where by there is loss of intercellular adherence
170
Q

What is pemphigoid?

A
  1. Term applied to a group of immune-mediated blistering diseases characterised by the production of autoantibodies to various components of the hemidesmosomes and epithelial basement membrane.
  2. These structures mediate attachment between epithelium and underlying connective tissue
  3. Their damage in pemphigoid results in formation of subepithelial vesicles
171
Q

What are key features of mucous membranes pemphigoid?

A
  1. Group of disorders affecting mainly women in the sixth decade of life
  2. Desquamative gingivitis can be a manifestation
  3. Nikolsky’s sign is typically positive
  4. Oral mucosa is often the first site
  5. Involvement of eyes may cause scarring and blindness
  6. Oral bullae are subepithelial and frequently seen intact (due to lid of full-thickness epithelium)
  7. When they rupture they give rise to erosion which heal slowly sometimes with scarring (thus the alternative name cicatricial pemphigoid)
171
Q

What is the management of mucous membrane pemphigoid?

A

Diagnosis
1. Direct immunofluorescne study of fresh unfixed biopsy material to detect tissue bound immune products (IgA and IgG to the basement membrane) from an intact bulla
Management
1. Ocular examination is necessary if early changes in the eyes as suspected
2. Can be effectively controlled with topical corticosteroids

172
Q

Describe the immunopathology of mucous membrane pemphigoid

A
  1. Adhesion of epithelium to connective tissue is mediated by the hemidesmosome (basement membrane complex)
  2. There are different combination of antibodies to the antigens found on the attachment proteins of the hemidesmosomes
  3. Destruction of the attachment protein leads to formation of pemphigoid lesions that show separation of the full thickness of the epithelium from the lamina propria (subepithelial bulla)
173
Q

What are key features of sialoliths (salivary calculi)?

A
  1. Usually formed by accretion of calcium salts around organic nidus
  2. Occurs about 80% in the submandibular gland
  3. Typically pain is caused at meal times when there is surge of salivary excretion and obstruction is encountered
  4. Occasionally asymptomatic until palpable in the mouth or seen in routine radiograph
  5. Do not cause dry mouth
  6. Should be removed by manipulation or incision of duct
174
Q

What is sialosis (sialadenosis)?

A
  1. A painless, non inflammatory, non neoplastic swelling of the salivary gland (most noticeably the parotids)
  2. Causes include
    a) Alcoholism
    b) Diabetes mellitus
    c) Bulimia
    d) Other endocrine disease
    e) Pregnancy
  3. Histologically, there is hypertrophy (increase in volume and size of cells) of serous acini
175
Q

What are the classical signs of malignant condition that should arouse immediate suspicion?

A
  1. Persistent ulceration: any unexplained ulcer that lasts for longer than 10 days should be treated with suspicion
  2. Induration: thickening and hardening of tissues
  3. Proliferative growth of tissue above its normal level: often with changes in the surface texture and colour changes
  4. Fixation of the affected tissue to the underlying structure

Oral Medicine (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions