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Dentaire > Chapter 1 to 13 OMII > Flashcards

Chapter 1 to 13 OMII Flashcards

Révisions Noémie

1
Q

What is dry socket (Alveolar osteitis)?

A

Postoperative pain inside and around the dental alveolus; often after dental extraction. Characterized by partial or total disintegration of the intra-alveolar blood clot and may cause halitosis.

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2
Q

What are the etiological factors of dry socket?

A

Difficulty of extraction; surgeon skill; oral contraceptives; insufficient cleaning of the socket; advanced age; female gender; smoking; excessive use of vasoconstrictors during anesthesia; immunosuppression.

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3
Q

What are the clinical features of dry socket?

A

Slight discomfort followed by intense pain; disintegration of the blood clot; exposed bone walls; separated gingival margins; possible halitosis; pain radiating to the ear and homolateral side of the head.

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4
Q

How to manage dry socket?

A

X-ray to rule out foreign body or bone destruction; pain control (NSAIDs; ibuprofen; dexketoprofen); dressing materials (Alvogyl); 0.2% chlorhexidine gluconate rinse; no antibiotic therapy needed.

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5
Q

What is osteomyelitis?

A

An infectious inflammatory disease of bone caused by bacterial colonization of the bone marrow; more common in the mandible due to its poor blood supply.

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6
Q

What are the etiological factors of osteomyelitis?

A

Malnutrition; alcoholism; diabetes; leukemia; anemia; irradiated bone; drugs; other bone diseases (Paget’s disease; florid osseous dysplasia); odontogenic infections; facial trauma with fractures; radiotherapy in the orofacial area.

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7
Q

What are the clinical features of acute osteomyelitis?

A

Pain; inflammation; exposed bone; cheek swelling; discharge; mobility of affected teeth; paresthesia of the alveolar nerve in the mandible.

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8
Q

How to manage osteomyelitis?

A

Antibiotic treatment (amoxicillin-clavulanic acid + fluocinolone); surgical drainage of pus; surgical debridement (sequestrectomy) in chronic phases.

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9
Q

What is osteoradionecrosis?

A

An area of necrotic bone exposed in an irradiated field; failing to heal for at least 3 months; often after radiotherapy in the head and neck region.

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10
Q

What are the etiological factors of osteoradionecrosis?

A

Radiotherapy induces inflammation of small blood vessels in the bone; forming thrombi; reducing tissue perfusion; producing free radicals that alter collagen synthesis; causing bone necrosis.

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11
Q

What are the clinical features of osteoradionecrosis?

A

Ulceration with exposure of necrotic bone; advanced sequestration; trismus; intense pain; swelling; cutaneous fistulas; and pathological fractures.

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12
Q

How to manage osteoradionecrosis?

A

Suppress mucosal irritants; optimize oral hygiene; chlorhexidine rinses; analgesics and antibiotics; curettage or debridement if pain persists; more radical surgery if necessary.

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13
Q

What is osteochemonecrosis?

A

A complication of bisphosphonate usage; characterized by transmucosal exposure of necrotic bone; often followed by infection and pain.

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14
Q

What are the risk factors of osteochemonecrosis?

A

Type of medication (bisphosphonates; RANK ligand inhibitors); duration of therapy; dentoalveolar surgery; anatomic factors; pre-existing dental disease; demographic and systemic factors.

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15
Q

What is odontogenic maxillary sinusitis?

A

Inflammation of the maxillary sinus membrane due to bacterial; viral infections; or allergic reactions; often caused by dental caries; trauma; extractions; periodontal disease.

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16
Q

What are the clinical features of acute maxillary sinusitis?

A

Pain in the orbital area; facial fullness; halitosis; nasal obstruction; purulent oro-sinus or nasal discharge.

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17
Q

How to diagnose odontogenic maxillary sinusitis?

A

Clinical features; radiographic findings (water projection); CT to show odontogenic origin; sinus puncture.

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18
Q

How to treat acute maxillary sinusitis?

A

Broad-spectrum antibiotics (amoxicillin-clavulanate); ibuprofen; extraction or endodontic treatment of associated teeth; prolonged antibiotics if necessary; surgical approach if no improvement.

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19
Q

What are odontogenic tumours (OT)?

A

A heterogenous group of lesions of diverse clinical behavior and histopathologic types; ranging from hamartomatous lesions to malignancy. Derived from ectomesenchymal and;or epithelial tissues constituting the tooth-forming apparatus.

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20
Q

What is the classification of OT according to WHO?

A
  1. Benign: Tumour of odontogenic epithelium; Mixed odontogenic tumour; Tumour of odontogenic ectomesenchyma. 2. Malignant: Odontogenic carcinoma; Odontogenic sarcoma.
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21
Q

What is an ameloblastoma?

A

The most common OT; locally aggressive growth; high recurrence rate. Occurs mostly between ages 20-40; commonly found in the third molar area; 75% in the mandible; 25% in the maxilla.

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22
Q

What are the clinical features of ameloblastoma?

A

Slow growth; asymptomatic bone expansion deformity; hard swelling; tooth mobility.

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23
Q

What are the radiographic features of ameloblastoma?

A

Unilocular or multilocular radiolucency (‘soap bubbles’ or ‘honeycomb’); well-defined margins; varying degrees of teeth root resorption.

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24
Q

How to manage ameloblastoma?

A

Wide excision; 20% recurrence rate.

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25
Q

What is a calcifying epithelial odontogenic tumour (Pindborg tumour)?

A

A rare OT (1%); occurs in ages 30-50 with no sex predilection; 6% are extraosseous; commonly found in the mandible; posterior area.

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26
Q

What are the clinical features of a calcifying epithelial odontogenic tumour?

A

Painless slow-growing swelling.

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27
Q

What are the radiographic features of a calcifying epithelial odontogenic tumour?

A

Lucent area with well or poorly defined multilocular radiopacities within the lesion.

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28
Q

How to manage a calcifying epithelial odontogenic tumour?

A

Total resection of the lesion; 20% recurrence rate; 15% for clear cell variant.

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29
Q

What is an adenomatoid odontogenic tumour?

A

A rare OT (3%); occurs in ages 10-20 with female predilection; considered a hamartoma.

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30
Q

What are the clinical features of an adenomatoid odontogenic tumour?

A

Asymptomatic slow-growing mass; 75% associated with an impacted tooth; commonly found in the anterior area.

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31
Q

What are the radiographic features of an adenomatoid odontogenic tumour?

A

Well-defined radiolucency with a sclerotic margin.

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32
Q

How to manage an adenomatoid odontogenic tumour?

A

Surgical removal with no recurrences.

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33
Q

What is a keratocystic odontogenic tumour?

A

A tumour affecting young adults (20-30 years); male predisposition; commonly found in the posterior mandible.

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34
Q

What are the clinical features of a keratocystic odontogenic tumour?

A

Slow growth; cortical expansion; tooth displacement; associated with Gorlin Goltz Syndrome (keratocysts; bone alterations; basal cell carcinomas).

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35
Q

What are the radiographic features of a keratocystic odontogenic tumour?

A

Unilocular or multilocular radiolucency; cortical expansion; tooth displacement; no root resorption except for third molars.

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36
Q

How to manage a keratocystic odontogenic tumour?

A

Surgical excision with curettage of the underlying bone; use of chemical products like Carney solution; marsupialization for large lesions; high recurrence rate.

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37
Q

What is an osteoma?

A

A benign osteogenic lesion characterized by excessive and persistent proliferation of bone with slow growth.

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38
Q

What are the clinical features of an osteoma?

A

Slow growth; painless; typically occurs in adults; often found in the mandible.

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39
Q

What are the radiographic features of an osteoma?

A

Well-defined radiopaque area.

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40
Q

What is Gardner Syndrome?

A

An autosomal dominant inherited syndrome with lesions derived from the three embryonic layers; including polyps with malignancy potential; craniofacial osteomas; teeth retention; supernumerary teeth; cement lesions; epidermoid cysts; fibromas; lipomas; and pigmented lesions.

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41
Q

What are osteoid osteoma and osteoblastoma?

A

Benign bony lesions closely related; differ in size and location. Osteoid osteoma is usually cortical; osteoblastoma is medullary.

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42
Q

What are the clinical features of osteoid osteoma?

A

Intermittent pain; intensity increases over time; nocturnal predominance; pain relieved with NSAIDs.

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43
Q

What are the radiographic features of osteoid osteoma?

A

Radiolucent area; well-circumscribed ‘nest’ < 1 cm; surrounded by reactive sclerotic bone; may contain radiopaque areas.

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44
Q

What are the clinical features of osteoblastoma?

A

Less intense pain without nocturnal predominance; does not respond to NSAIDs; adjacent teeth mobility.

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45
Q

What are the radiographic features of osteoblastoma?

A

Osteolytic area with calcified material inside; > 2 cm; may expand or erode cortices.

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46
Q

What is an osteochondroma?

A

A benign tumor characterized by the formation of mature cartilage; typically occurs in tubular bones and is rare in the jaw.

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47
Q

What are the clinical features of an osteochondroma?

A

Painless slow-growing tumor; may cause dental mobility.

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48
Q

What are the radiographic features of an osteochondroma?

A

Radiolucent irregular areas.

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49
Q

What is an osteosarcoma?

A

The most common primary bone tumor; occurs typically in the 3rd to 4th decade; more common in men; associated with rapid growing swelling; pain; anesthesia or paresthesia; teeth exfoliation; and pathological fractures.

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50
Q

What are the clinical features of an osteosarcoma?

A

Rapidly growing swelling; painful; anesthesia or paresthesia; exfoliation of teeth; pathological fractures.

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51
Q

What are the radiographic features of an osteosarcoma?

A

Destructive bone lesion; ‘sunray appearance;’ symmetrical widening of the periodontal ligament.

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52
Q

What is a chondrosarcoma?

A

A malignant neoplasm forming a cartilaginous matrix but no bone; typically occurs in the 5th to 6th decade; more common in the mandible (premolar; molar regions).

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53
Q

What are the clinical features of a chondrosarcoma?

A

Rapidly growing tumor; later metastases.

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54
Q

What are the radiographic features of a chondrosarcoma?

A

Poorly defined radiolucency.

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55
Q

What is a peripheral giant cell granuloma?

A

A tissue reactive hyperplasia of the oral mucosa; commonly found on the gingival margins in the anterior part of the mouth; affecting mostly females aged 40-60.

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56
Q

What are the clinical features of a peripheral giant cell granuloma?

A

Broad-based; sessile; purplish-red elevation of the mucosa; usually ≥ 1cm in size.

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57
Q

What are the radiographic features of a peripheral giant cell granuloma?

A

Non-specific radiolucent area; resorption of the alveolar crest; widening of the periodontal space.

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58
Q

What is a central giant cell granuloma?

A

A benign tumour of osteoclastic origin; not unique to the jaws or odontogenic; more common in women aged 10-30.

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59
Q

What are the clinical features of a central giant cell granuloma?

A

Painless swelling that can displace teeth; rare paresthesia; ability to expand and perforate cortical bone; resorbs roots; often crosses the midline in the anterior mandible region.

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60
Q

What are the radiographic features of a central giant cell granuloma?

A

Well-defined; sometimes multilocular radiolucent area; crossed midline; thin cortices; displaced teeth; resorbed roots.

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61
Q

What is an aneurysmal bone cyst?

A

Not a true cyst except in x-ray appearance; often due to vascular malformations; more common in young female patients; found in the posterior mandible.

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62
Q

What are the clinical features of an aneurysmal bone cyst?

A

Painful swelling.

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63
Q

What are the radiographic features of an aneurysmal bone cyst?

A

Multilocular radiolucency; cortical expansion.

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64
Q

What is hyperparathyroidism (Brown tumour)?

A

Resulting from overproduction of parathyroid hormone; characterized by increased calcium blood levels; commonly affects middle-aged individuals.

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65
Q

What is cherubism?

A

A non-neoplastic bone disease characterized by painless bilateral swelling of the jaws; autosomal dominant with variable expressivity; affecting mostly males (100%) and females (50-70%).

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66
Q

What are the clinical features of cherubism?

A

Symmetrical mandibular swellings (chubby face) beginning from ages 2 to 7; maxillary involvement causing eyes to turn upwards.

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67
Q

What are the radiographic features of cherubism?

A

Multilocular cysts; reduced thickness of bony cortices; diffuse rarefaction in the maxilla.

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68
Q

What is an ossifying fibroma?

A

A slow-growing neoplasm well-circumscribed; constituted by cellular fibrous tissue containing calcified centers resembling bone or cement.

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69
Q

What are the clinical features of an ossifying fibroma?

A

Common in women in their 3rd or 4th decade; often found in the mandible (70-90%); asymptomatic or causing discomfort; capable of producing cortical expansion and functional deformity.

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70
Q

What are the radiographic features of an ossifying fibroma?

A

Initial phase: well-circumscribed unilocular radiolucent area; Intermediate phase: radiolucent-radiopaque areas; Last phase: radiopaque.

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71
Q

What is fibrous dysplasia?

A

Bone replacement by fibrous tissue of unknown etiology; equally affects males and females; can be monostotic (one bone) or polyostotic (many bones).

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72
Q

What are the clinical features of fibrous dysplasia?

A

Monostotic: involves young adults (20-35 years); affecting one bone (maxilla or mandible); unilateral swelling causing facial deformity; slow growth; painless; dental displacement and malocclusion. Polyostotic: affects children with multiple bones and pigmented lesions; associated with endocrine alterations.

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73
Q

What is Paget’s disease of bone?

A

Also known as osteitis deformans; it is characterized by anarchic osteoclastic and osteoblastic activity leading to distortion and weakening of bones; typically occurring later in life.

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74
Q

What are the etiological factors of Paget’s disease?

A

Unknown etiology; potentially viral; with genetic susceptibility (mutation P3921-P62).

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75
Q

What are the clinical features of Paget’s disease?

A

Higher prevalence with age (over 50 years); begins in a single bone but 90% become polyostotic. Active and inactive stages; affects main bones like lumbar vertebrae; sacrum; skull; femur; and tibia. Causes bone thickening; enlargement; and distortion; involvement of skull bones can cause deafness and nerve alterations.

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76
Q

What are the radiographic features of Paget’s disease?

A

Loss of normal trabecular pattern with areas of radiolucency replaced by cotton wool appearance. Early stages show loss of lamina dura and resorption of periapical bone; later stages show hypercementosis and mixed radiolucent and radiopaque areas.

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77
Q

What are the histological features of Paget’s disease?

A

Bone resorption and repair with osteoclastic resorption and fibrovascular proliferation. Osteoblasts lay down new bone within a vascular stroma.

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78
Q

What are the chemical findings in Paget’s disease?

A

Increased levels of alkaline phosphatase; hydroxyproline; and hypercalcemia.

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79
Q

What is the prognosis of Paget’s disease?

A

Typically active for 3-5 years before becoming static; can cause oral complications like problems with dentures; bleeding; and bone infections.

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80
Q

How is Paget’s disease treated?

A

Oral bisphosphonates are commonly used.

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81
Q

What is Langerhans cell histiocytosis?

A

A disorder characterized by the proliferation of Langerhans cells; with 10% oral involvement; mostly in the mandible (73%).

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82
Q

What are the forms of Langerhans cell histiocytosis?

A
  1. Solitary eosinophilic granuloma; 2. Multifocal eosinophilic granuloma; 3. Letterer-Siwe disease.
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83
Q

What are the clinical features of solitary eosinophilic granuloma?

A

Affects adults; causes destruction; pain; and swelling of a bone; gross periodontal destruction; root exposure; and in 10% of patients; loosened teeth.

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84
Q

What are the radiographic features of solitary eosinophilic granuloma?

A

Well-defined round area of radiolucency; commonly in alveolar ridges and mandible; teeth appear floating in air.

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85
Q

What are the clinical features of multifocal eosinophilic granuloma?

A

Involves the mandible; other bones; and sometimes viscera and skin. Associated with skull; axial skeleton; and femora; and can cause Hand-Schüller-Christian triad (exophthalmos; diabetes insipidus; lytic skull lesions).

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86
Q

What are the clinical features of Letterer-Siwe disease?

A

Affects infants and young children; involving bones and soft tissues. Symptoms include lymphadenopathy; splenomegaly; fever; anemia; thrombocytopenia; infections; and rashes.

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87
Q

What are the radiographic features of Langerhans cell histiocytosis?

A

Bone lesions similar to those in Langerhans cell histiocytosis.

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88
Q

What is the prognosis of Langerhans cell histiocytosis?

A

Isolated lesions may regress spontaneously; widespread disease can be fatal with a mortality rate of 15-50%.

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89
Q

How is Langerhans cell histiocytosis diagnosed?

A

Diagnosis is confirmed through biopsy and immunohistochemistry showing Langerhans cells; protein S100; and CD1.

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90
Q

How is Langerhans cell histiocytosis treated?

A

Treatment options include curettage; intra-lesional corticosteroid injections; and irradiation of active bone lesions.

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91
Q

What is Paget’s disease of bone?

A

Also known as osteitis deformans; it is characterized by anarchic osteoclastic and osteoblastic activity leading to distortion and weakening of bones; typically occurring later in life.

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92
Q

What are the etiological factors of Paget’s disease?

A

Unknown etiology; potentially viral; with genetic susceptibility (mutation P3921-P62).

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93
Q

What are the clinical features of Paget’s disease?

A

Higher prevalence with age (over 50 years); begins in a single bone but 90% become polyostotic. Active and inactive stages; affects main bones like lumbar vertebrae; sacrum; skull; femur; and tibia. Causes bone thickening; enlargement; and distortion; involvement of skull bones can cause deafness and nerve alterations.

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94
Q

What are the radiographic features of Paget’s disease?

A

Loss of normal trabecular pattern with areas of radiolucency replaced by cotton wool appearance. Early stages show loss of lamina dura and resorption of periapical bone; later stages show hypercementosis and mixed radiolucent and radiopaque areas.

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95
Q

What are the histological features of Paget’s disease?

A

Bone resorption and repair with osteoclastic resorption and fibrovascular proliferation. Osteoblasts lay down new bone within a vascular stroma.

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96
Q

What are the chemical findings in Paget’s disease?

A

Increased levels of alkaline phosphatase; hydroxyproline; and hypercalcemia.

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97
Q

What is the prognosis of Paget’s disease?

A

Typically active for 3-5 years before becoming static; can cause oral complications like problems with dentures; bleeding; and bone infections.

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98
Q

How is Paget’s disease treated?

A

Oral bisphosphonates are commonly used.

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99
Q

What is Langerhans cell histiocytosis?

A

A disorder characterized by the proliferation of Langerhans cells; with 10% oral involvement; mostly in the mandible (73%).

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100
Q

What are the forms of Langerhans cell histiocytosis?

A
  1. Solitary eosinophilic granuloma; 2. Multifocal eosinophilic granuloma; 3. Letterer-Siwe disease.
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101
Q

What are the clinical features of solitary eosinophilic granuloma?

A

Affects adults; causes destruction; pain; and swelling of a bone; gross periodontal destruction; root exposure; and in 10% of patients; loosened teeth.

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102
Q

What are the radiographic features of solitary eosinophilic granuloma?

A

Well-defined round area of radiolucency; commonly in alveolar ridges and mandible; teeth appear floating in air.

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103
Q

What are the clinical features of multifocal eosinophilic granuloma?

A

Involves the mandible; other bones; and sometimes viscera and skin. Associated with skull; axial skeleton; and femora; and can cause Hand-Schüller-Christian triad (exophthalmos; diabetes insipidus; lytic skull lesions).

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104
Q

What are the clinical features of Letterer-Siwe disease?

A

Affects infants and young children; involving bones and soft tissues. Symptoms include lymphadenopathy; splenomegaly; fever; anemia; thrombocytopenia; infections; and rashes.

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105
Q

What are the radiographic features of Langerhans cell histiocytosis?

A

Bone lesions similar to those in Langerhans cell histiocytosis.

106
Q

What is the prognosis of Langerhans cell histiocytosis?

A

Isolated lesions may regress spontaneously; widespread disease can be fatal with a mortality rate of 15-50%.

107
Q

How is Langerhans cell histiocytosis diagnosed?

A

Diagnosis is confirmed through biopsy and immunohistochemistry showing Langerhans cells; protein S100; and CD1.

108
Q

How is Langerhans cell histiocytosis treated?

A

Treatment options include curettage; intra-lesional corticosteroid injections; and irradiation of active bone lesions.

109
Q

What is sialadenitis?

A

Non-neoplastic swelling of salivary glands due to bacterial; viral; ionising radiation; obstructive; or immunological causes; commonly affecting the parotid and submandibular glands.

110
Q

What are the modifiable risk factors for sialadenitis?

A

Dehydration; recent surgery and anesthesia; malnutrition; medications (e.g.; antihistamines; diuretics; tricyclic antidepressants); sialolithiasis; oral infections.

111
Q

What are the non-modifiable risk factors for sialadenitis?

A

Advanced age; radiation therapy without cytoprotective agents; renal failure; hepatic failure; congestive heart failure; HIV;AIDS; diabetes mellitus; anorexia nervosa;bulimia; cystic fibrosis; Cushing’s disease.

112
Q

What are the clinical features of viral sialadenitis caused by mumps?

A

Caused by the paramyxovirus; common in children (6-8 years); characterized by fever; malaise; headache; pre-auricular tenderness; painful parotid gland enlargement; redness; tenderness; and trismus. It resolves in 7-10 days without sequelae but can cause complications like epididymo-orchitis or oophoritis.

113
Q

What are the clinical features of HIV;AIDS-associated sialadenitis?

A

Diffuse enlargement of the salivary glands at any stage of HIV infection; characterized by non-tender persistent swelling; decreased salivary flow.

114
Q

What are the clinical features of acute bacterial sialadenitis?

A

Characterized by unilateral or bilateral salivary gland enlargement; diffuse painful swelling; indurated and tender glands; warm and red skin over the gland; possible purulent discharge; trismus; xerostomia; fever; and malaise.

115
Q

What are the treatment options for acute bacterial sialadenitis?

A

Immediate IV amoxicillin-clavulanic acid every 6 hours; surgical decompression by external drainage in severe or refractory cases; or with an obvious abscess.

116
Q

What are the clinical features of recurrent bacterial sialadenitis?

A

Recurrent episodes of unilateral or bilateral parotid swelling; pain in the pre-auricular area; sometimes purulent saliva upon squeezing of the gland; frequent in parotid glands.

117
Q

What are the diagnostic methods for recurrent bacterial sialadenitis?

A

Clinical manifestations; repeated episodes of swelling with few symptoms; sialography showing rosary or birdshot images; MRI.

118
Q

What are the treatment options for recurrent bacterial sialadenitis?

A

Antibiotic treatment (875;125mg amoxicillin-clavulanic acid every 8 hours; 300mg clindamycin every 8 hours); analgesics (paracetamol; ibuprofen); hydration; surgical intervention in severe cases.

119
Q

What is obstructive sialadenitis (sialolithiasis)?

A

The most frequent pathology of the salivary gland caused by calculus (sialolith) or other factors like congenital malformations; inflammation; or autoimmune alterations.

120
Q

What are the clinical features of obstructive sialadenitis?

A

Intense pain that increases when eating; swelling; signs of secondary infection; purulent exudate from the excretory duct; firm and painful gland on palpation; possible fever; malaise; and mild to moderate leucocytosis.

121
Q

What are the diagnostic methods for obstructive sialadenitis?

A

Palpation if superficial; occlusal radiography if calcified; sialography to show interruption of contrast passage; echographs; CT; MRI for acute sialadenitis.

122
Q

What are the treatment options for obstructive sialadenitis?

A

Antibiotics; analgesics; hydration; removal of calculus if located near the duct outlet; surgical removal if obstruction persists; radical surgery of the gland if calculus is deep or symptomatology persists.

123
Q

What is radiation sialadenitis?

A

Inflammation of salivary glands due to external irradiation or radiodine therapy; leading to atrophy and transient or permanent oral dryness.

124
Q

What are the clinical features of radiation sialadenitis?

A

Xerostomia with hyposialia; burning of the tongue; frequently combined with hypogeusia or ageusia; some recovery over years; but many patients experience persistent complaints.

125
Q

What are the treatment options for radiation sialadenitis?

A

Treatment of associated symptoms; preventive measures to reduce risk of complications; pilocarpine (Salagen) 5mg 3 times a day for hyposialia.

126
Q

What is necrotizing sialometaplasia?

A

A benign disease process that mimics cancer; characterized by vascular ischemia caused by embolism; often triggered by local trauma like anesthetic injection; tobacco; or alcohol. It presents as ulcerated or exophytic forms and heals spontaneously within 3 months.

127
Q

What is sialadenosis (sialosis)?

A

Enlargement of the salivary glands (parotid); characterized by bilateral; non-inflammatory; non-neoplastic; soft; symmetrical; painless; and persistent swelling.

128
Q

What are the conditions associated with sialadenosis?

A

Endocrine disorders (diabetes mellitus; hypothyroidism; pregnancy; lactation; puberty; menopause; adrenal gland disorders); metabolic disorders (alcoholism; liver cirrhosis; malnutrition; bulimia; anorexia; obesity; vitamin deficiency); autoimmune disorders (Sjögren syndrome); and drugs (antihypertensives; psychotropics; atropine; naproxen; benzodiazepines).

129
Q

What are the clinical features of sialadenosis?

A

No sex predilection; highest incidence in people aged 40-70; non-inflammatory with no suppuration; slowly evolving and recurrent swelling; painless; soft to palpation; long evolution (20 years).

130
Q

How is sialadenosis diagnosed?

A

Clinical diagnosis based on bilateral; painless; progressive growth; MRI; CT; fine-needle aspiration (FNA); biopsy showing hypertrophy of the acini and compression of the ducts.

131
Q

What are the treatment options for sialadenosis?

A

Causal treatment (control diabetes; alcoholism; remove or replace drug); aesthetic treatment (superficial parotidectomies if requested by the patient); pilocarpine 1.25-5mg;day orally for bulimia;anorexia.

132
Q

What is Sjögren syndrome?

A

A chronic systemic autoimmune disease affecting exocrine glands; characterized by lymphocytic inflammatory infiltrate that destroys glands leading to xerostomia and xerophthalmia.

133
Q

What are the clinical forms of Sjögren syndrome?

A

Primary SS: keratoconjunctivitis sicca and hyposialia. Secondary SS: presence of connective tissue disease (rheumatoid arthritis; systemic lupus erythematosus; myositis; systemic sclerosis).

134
Q

What are the aetiopathogenesis factors for Sjögren syndrome?

A

Multifactorial and complex; involving endocrine and genetic factors; certain viruses (Cytomegalovirus; Epstein Barr; Herpes); and alterations in cell apoptosis regulation.

135
Q

What are the clinical features of Sjögren syndrome?

A

Fatigue; mild arthralgia; dry eye (xerophthalmia); decreased tears; pain; photosensitivity; difficulties in speech; chewing; and swallowing; dry mouth sensation (xerostomia); taste alterations; burning sensation.

136
Q

What are the clinical signs of Sjögren syndrome?

A

Cracked; dry; and desquamative lips; dry; erythematous; and fissured tongue; rampant caries in atypical locations; gland swelling; mucositis; oral ulcerations; chronic erythematous candidiasis; periodontal diseases.

137
Q

What are the extra glandular symptoms of Sjögren syndrome?

A

Musculoskeletal (myalgia; arthralgia; arthritis); respiratory (interstitial-like disease); gastrointestinal (dysphagia; liver involvement; autoimmune hepatitis); urinary (nephritis; glomerulonephritis); vessels and skin (Reynaud’s phenomenon; vasculitis; purpura; annular erythema); neurological (peripheral sensory or motor neuropathy; cranial neuropathy); psychiatric (depression; anxiety); cardiac (pericarditis).

138
Q

What is the most serious complication of Sjögren syndrome?

A

The most serious complication is parotid gland lymphomas. 5% of patients develop non-Hodgkin lymphoma (NHL); with a 44-fold greater risk than the general population.

139
Q

How is Sjögren syndrome diagnosed?

A

Diagnosis includes the ACR-EULAR classification criteria for primary Sjögren’s syndrome; requiring at least one symptom of ocular or oral dryness; and complementary diagnostic techniques like lower lip minor salivary gland biopsy.

140
Q

What is the ACR-EULAR classification criteria for primary Sjögren’s syndrome?

A

Inclusion criteria: at least one symptom of ocular or oral dryness. Eye symptoms: dry eye sensation; sand in the eyes sensation; need for artificial tear drops at least three times a day. Oral symptoms: dry mouth sensation; persistent or recurrent salivary gland enlargement; need to drink liquid to swallow food.

141
Q

What are the exclusion criteria for Sjögren syndrome diagnosis?

A

Exclusion criteria: history of head and neck radiation treatment; active hepatitis C infection; acquired immunodeficiency syndrome; sarcoidosis; amyloidosis; graft versus host disease; IgG4-related disease.

142
Q

What are the complementary diagnostic techniques for Sjögren syndrome?

A

Lower lip minor salivary gland biopsy to determine focus score. A positive biopsy for SS shows a focus score ≥ 1; with a focus being an aggregate of over 50 lymphocytes in 4 mm2 of gland tissue.

143
Q

What are the treatment options for xerophthalmia in Sjögren syndrome?

A

Xerophthalmia treatment includes artificial tears; antibiotic eye drops for conjunctivitis; and pilocarpine (Salagen) 5mg three times a day.

144
Q

What are the treatment options for xerostomia in Sjögren syndrome?

A

Xerostomia treatment includes frequent small sips of water; sugar-free gums; saliva substitutes (carboxymethyl cellulose solution: Oral Balance); and pilocarpine (Salagen) to stimulate gland function. Oral hygiene maintenance; fluoride applications; chlorhexidine rinses; restorative teeth treatments; and nystatin solutions for candidiasis.

145
Q

What is a mucocele?

A

Cystic formations containing mucin; primarily from minor salivary glands and the sublingual gland; caused by mucous escape or retention.

146
Q

What are the aetiologies of mucoceles?

A

Mucous escape reaction (80-90% due to trauma); mucous retention (chronic irritation); more common in childhood and adolescence for escape; and in adults over 40 for retention.

147
Q

What are the clinical features of mucoceles?

A

Well-defined swelling; asymptomatic or mild symptoms; mucosa similar in color to normal or bluish; located on lower lip; buccal mucosa; tongue; and palate; fluctuates in size; can interfere with mastication and speaking; recurrent.

148
Q

How are mucoceles diagnosed?

A

Clinical diagnosis; fine-needle aspiration (FNA); CT;MR; excisional biopsy.

149
Q

What is the treatment for mucoceles?

A

Excision of the mucocele and the injured minor salivary gland; ensuring complete removal to prevent recurrence.

150
Q

What is a ranula?

A

A cyst of salivary retention exclusively in the sublingual gland.

151
Q

What are the aetiologies of ranulas?

A

Malformation of the duct system; trauma; infection.

152
Q

What are the clinical features of ranulas?

A

Asymptomatic swelling with progressive growth; fluctuates in size; located on the floor of the mouth; may cross the midline; can burst releasing saliva.

153
Q

How are ranulas diagnosed?

A

Clinical diagnosis; FNA; CT;MR; excisional biopsy.

154
Q

What is the treatment for ranulas?

A

Surgical excision.

155
Q

What are the general features of salivary gland tumours?

A

1% of body tumours; 5% of head and neck tumours; most common in the 6th-7th decade; no sex predilection; 80% in parotid gland; 10% submandibular; 9% minor salivary glands; 1% sublingual.

156
Q

What are the clinical features of benign salivary gland tumours?

A

Slow-growing mass; not fixed to surrounding tissues; asymptomatic; not ulcerated.

157
Q

What are the clinical features of malignant salivary gland tumours?

A

Fast-growing mass; fixed to skin and surrounding tissues; hard consistency; painful; may be ulcerated.

158
Q

What is the TNM staging system for salivary gland tumours?

A

TNM system: Tumour (T) size and location; Node (N) lymph node involvement; Metastasis (M) spread to other body parts.

159
Q

How are salivary gland tumours diagnosed?

A

Medical record; clinical examination (size; consistency; skin and mucosa color); imaging tests (CT; MRI; orthopantomography; echography; scintigraphy; sialography); histopathology (FNA; intra-operatory biopsy).

160
Q

What are the treatment options for salivary gland tumours?

A

Surgery (tumour resection with security margins; no neck dissection needed); radiotherapy (RT) for incomplete resection; lymph node metastases; recurrent lesions; chemotherapy (CT) for inoperable tumours.

161
Q

What is the WHO classification of salivary gland tumours (2005)?

A

Epithelial tumours: adenomas (pleomorphic adenoma; myoepithelioma; basal cell adenoma; Whartin’s tumour; oncocytoma; canalicular adenoma; sebaceous adenoma; lymphadenoma; ductal papilloma; cystadenoma); carcinomas (acinic cell carcinoma; mucoepidermoid carcinoma; adenoid cystic carcinoma; polymorphous low-grade adenocarcinoma; epithelial-myoepithelial carcinoma; clear cell carcinoma; basal cell adenocarcinoma; adenocarcinoma basal cells; sebaceous lymphadenocarcinoma; cystadenocarcinoma). Non-epithelial tumours: lymphomas; metastases to parotid lymph nodes.

162
Q

What are the characteristics of pleomorphic adenoma?

A

Most frequent benign tumour (80%); primarily in parotid gland (75%); more common in women (4:1); peak age 40. Slow-growing lobulated swelling; asymptomatic; well-delimitated; not fixed to underlying tissues; no facial palsy.

163
Q

What are the chief complaints in neuromuscular examination in dentistry?

A

Pain; decrease or loss of sensitivity; paralysis.

164
Q

What are the key aspects of the clinical examination in neuromuscular dentistry?

A

Intraoral examination (lips; cheeks; palate; tongue; floor of the mouth; gums; teeth; tonsils; pharynx); application of stimuli; occlusion assessment.

165
Q

What stimuli are used in neuromuscular examination?

A

Thermal; chemical; mechanical; or electrical stimuli; and percussion of teeth.

166
Q

What is examined in the temporomandibular joint (TMJ) clinical examination?

A

Range of opening; articular noises; deviations on opening or closing; palpation for clicks or crepitus.

167
Q

What are the signs of TMJ issues during palpation?

A

Palpation for clicks or crepitus; both sides at the same time; during rest and movement.

168
Q

How is posterior TMJ palpation performed?

A

With the little finger placed in the external auditory meatus; applying pressure forwards.

169
Q

What is the significance of auscultation in TMJ examination?

A

Auscultation with a stethoscope placed in the preauricular area to detect joint sounds.

170
Q

What are the types of noises associated with TMJ disorders?

A

Clicks indicate disc displacement; crepitus indicates osteoarthrosis of the TMJ.

171
Q

What muscles are included in the masticatory muscles examination?

A

Masseter; temporalis; medial pterygoid; lateral pterygoid; digastric; sternocleidomastoid.

172
Q

How is sensitivity to muscle palpation assessed?

A

Sensitivity to muscle palpation is assessed bilaterally in movement and rest; starting with muscle insertions.

173
Q

What are the functions of the masseter muscle?

A

Elevates the mandible; retracts the mandible; and performs lateral movements.

174
Q

What are the functions of the temporalis muscle?

A

Involved in crushing food.

175
Q

What are the roles of the internal and external pterygoid muscles?

A

External pterygoid pulls the head of the mandible forward to open the mouth; internal pterygoid elevates the mandible to close the mouth and performs lateral movements.

176
Q

What are the signs of masticatory muscle pain?

A

Sensitivity to muscle palpation; pain during bilateral palpation in movement and rest.

177
Q

Which cranial nerves are tested in neuromuscular examination?

A

I Olfactory; II Optic; III Oculomotor; IV Trochlear; V Trigeminal; VI Abducens; VII Facial; VIII Vestibulocochlear; IX Glossopharyngeal; X Vagus; XI Spinal Accessory; XII Hypoglossal.

178
Q

What are the sensory and motor functions of the trigeminal nerve (V)?

A

Sensory: face sensitivity; motor: mastication.

179
Q

How is the corneal reflex tested?

A

By touching the cornea with a cotton swab while the patient looks to the side; eliciting an involuntary blink.

180
Q

How is the motor function of the trigeminal nerve assessed?

A

By palpating the masseter and temporalis muscles while the patient clenches the mouth; asking the patient to squeeze the jaws while the examiner tries to separate them; pressing down on the chin.

181
Q

What are the functions of the facial nerve (VII)?

A

Motor: supplies muscles of facial expression; posterior belly of digastric muscle; stylohyoid; and stapedius. Sensory: taste from the anterior two-thirds of the tongue; hard and soft palates.

182
Q

How is the sensory function of the facial nerve tested?

A

Taste from the anterior two-thirds of the tongue; hard and soft palates.

183
Q

How is the motor function of the facial nerve tested?

A

Motor function is tested by asking the patient to raise both eyebrows; close both eyes tightly; show both upper and lower teeth; smile; and puff out both cheeks.

184
Q

What are the sensory and motor functions of the glossopharyngeal nerve (IX)?

A

Sensory: taste in the posterior one-third of the tongue; sensitivity of the middle ear and Eustachian tube. Motor: stylopharyngeus muscle; pharynx; and soft palate muscles.

185
Q

What are the sensory and motor functions of the vagus nerve (X)?

A

Sensory: taste from the base of the tongue and epiglottis; general sensation to the soft palate and upper larynx. Motor: larynx (speech) and esophagus (swallowing).

186
Q

How is the motor function of the spinal accessory nerve (XI) tested?

A

By assessing swallowing; head and neck movement; and movement of the upper shoulders.

187
Q

What are the motor functions of the hypoglossal nerve (XII)?

A

Controls muscles of the tongue; assessed by asking the patient to stick out the tongue in the midline and move it back and forth; push the tongue against the cheek while the examiner tests the force by pushing from outside the cheek.

188
Q

What is Burning Mouth Syndrome (BMS)?

A

A condition characterized by burning; stinging sensations in the oral mucosa; bilateral; continuous for at least 3 months; with improvement from food and drink; and associated taste alteration and;or xerostomia.

189
Q

What are the primary characteristics of BMS?

A

Bilateral burning or stinging in the oral mucosa; continuous for at least 3 months; no clinical lesions; improves with food and drink.

190
Q

What is the incidence of BMS?

A

0.7-2.6% of the population.

191
Q

Which demographic is most affected by BMS?

A

People aged 50-70; with an 8:1 female to male ratio.

192
Q

What are the etiological factors of idiopathic BMS?

A

Idiopathic BMS has no known cause; often linked to neuropathic pain due to peripheral or central receptor dysfunction.

193
Q

What is the neuropathic component of BMS?

A

Involves significant loss of epithelial and subepithelial nerve fibers; and alteration of nervous impulses in the trigeminal system.

194
Q

What are the etiological factors of secondary BMS?

A

Local factors; systemic problems; and psychogenic causes.

195
Q

What local factors contribute to secondary BMS?

A

Tongue thrusting; restricted tongue space from poor denture construction.

196
Q

What systemic problems are associated with secondary BMS?

A

Haematological deficiency states; diabetes; mucosal diseases.

197
Q

What psychogenic causes are linked to BMS?

A

Anxiety; accounting for 20% of cases.

198
Q

Which areas are most frequently affected by BMS?

A

Tongue; palate; lips; lower alveolus; usually bilateral.

199
Q

What are the clinical features of BMS?

A

Bilateral; no clinical signs of disease; relief with eating and drinking; increases as the day progresses.

200
Q

What are the common locations for BMS symptoms?

A

Multicentric: tongue; lips; palate; gums.

201
Q

What are the signs and symptoms associated with BMS?

A

Xerostomia; taste alterations; atypical dental pain; continuous movement of the tongue and lips.

202
Q

How is BMS diagnosed?

A

Absence of objective signs that justify the symptoms; sialometry; blood analysis for secondary BMS; allergy tests.

203
Q

What objective signs need to be absent for a BMS diagnosis?

A

No objective signs like glossitis; lichen planus; candidiasis; or xerostomia.

204
Q

What tests are undertaken to exclude systemic diseases in BMS diagnosis?

A

Laboratory tests to exclude systemic diseases.

205
Q

What are the primary steps in managing BMS?

A

Informing the patient about the condition and its management.

206
Q

What local drug treatments are used for BMS?

A

Local treatments include clonazepam (Rivotril); capsaicin combined with lidocaine; benzodiazepines.

207
Q

What systemic drug treatments are used for BMS?

A

Systemic treatments include clonazepam; antidepressants; benzodiazepines; gabapentin; alpha-lipoic acid.

208
Q

What is the role of clonazepam in BMS treatment?

A

Clonazepam is used for its calming effect and to reduce nerve-related pain.

209
Q

How does capsaicin help in BMS treatment?

A

Capsaicin is used for its pain relief properties by desensitizing sensory receptors.

210
Q

What are the benefits of alpha-lipoic acid in BMS management?

A

Alpha-lipoic acid is an antioxidant that helps in reducing nerve pain.

211
Q

What is the importance of informing the patient about BMS?

A

It is important to inform the patient about the nature of BMS; its chronic course; and the treatment options available to manage symptoms.

212
Q

Why is it necessary to exclude conditions like glossitis; lichen planus; and candidiasis in BMS diagnosis?

A

These conditions need to be excluded as they can cause similar symptoms to BMS and require different treatments.

213
Q

What are the primary characteristics of BMS?

A

Bilateral burning or stinging in the oral mucosa; continuous for at least 3 months; no clinical lesions; improves with food and drink.

214
Q

What is the incidence of BMS?

A

0.7-2.6% of the population.

215
Q

Which demographic is most affected by BMS?

A

People aged 50-70; with an 8:1 female to male ratio.

216
Q

What are the etiological factors of idiopathic BMS?

A

Idiopathic BMS has no known cause; often linked to neuropathic pain due to peripheral or central receptor dysfunction.

217
Q

What is the neuropathic component of BMS?

A

Involves significant loss of epithelial and subepithelial nerve fibers; and alteration of nervous impulses in the trigeminal system.

218
Q

What are the etiological factors of secondary BMS?

A

Local factors; systemic problems; and psychogenic causes.

219
Q

What local factors contribute to secondary BMS?

A

Tongue thrusting; restricted tongue space from poor denture construction.

220
Q

What systemic problems are associated with secondary BMS?

A

Haematological deficiency states; diabetes; mucosal diseases.

221
Q

What psychogenic causes are linked to BMS?

A

Anxiety; accounting for 20% of cases.

222
Q

Which areas are most frequently affected by BMS?

A

Tongue; palate; lips; lower alveolus; usually bilateral.

223
Q

What are the clinical features of BMS?

A

Bilateral; no clinical signs of disease; relief with eating and drinking; increases as the day progresses.

224
Q

What are the common locations for BMS symptoms?

A

Multicentric: tongue; lips; palate; gums.

225
Q

What are the signs and symptoms associated with BMS?

A

Xerostomia; taste alterations; atypical dental pain; continuous movement of the tongue and lips.

226
Q

How is BMS diagnosed?

A

Absence of objective signs that justify the symptoms; sialometry; blood analysis for secondary BMS; allergy tests.

227
Q

What objective signs need to be absent for a BMS diagnosis?

A

No objective signs like glossitis; lichen planus; candidiasis; or xerostomia.

228
Q

What tests are undertaken to exclude systemic diseases in BMS diagnosis?

A

Laboratory tests to exclude systemic diseases.

229
Q

What are the primary steps in managing BMS?

A

Informing the patient about the condition and its management.

230
Q

What local drug treatments are used for BMS?

A

Local treatments include clonazepam (Rivotril); capsaicin combined with lidocaine; benzodiazepines.

231
Q

What systemic drug treatments are used for BMS?

A

Systemic treatments include clonazepam; antidepressants; benzodiazepines; gabapentin; alpha-lipoic acid.

232
Q

What is the role of clonazepam in BMS treatment?

A

Clonazepam is used for its calming effect and to reduce nerve-related pain.

233
Q

How does capsaicin help in BMS treatment?

A

Capsaicin is used for its pain relief properties by desensitizing sensory receptors.

234
Q

What are the benefits of alpha-lipoic acid in BMS management?

A

Alpha-lipoic acid is an antioxidant that helps in reducing nerve pain.

235
Q

What is the importance of informing the patient about BMS?

A

It is important to inform the patient about the nature of BMS; its chronic course; and the treatment options available to manage symptoms.

236
Q

Why is it necessary to exclude conditions like glossitis; lichen planus; and candidiasis in BMS diagnosis?

A

These conditions need to be excluded as they can cause similar symptoms to BMS and require different treatments.

237
Q

What is the primary treatment goal for BMS?

A

The primary treatment goal for BMS is to manage symptoms and improve the patient’s quality of life.

238
Q

What are trigeminal neuropathies?

A

Disorders of sensation in the area of innervation of the trigeminal nerve.

239
Q

What are the types of sensation disorders in trigeminal neuropathies?

A

Partial sensibility loss (hypoesthesia); total sensibility loss (anesthesia); abnormal sensations (paresthesia;dysesthesia).

240
Q

What are the methods used in the clinical examination of the trigeminal nerve?

A

Light touch using a cotton wisp or tissue paper; pain using a needle.

241
Q

What are the etiopathogenic factors of trigeminal neuropathies?

A

Traumatism; tumors; collagen diseases; benign trigeminal neuropathy; infections; other causes.

242
Q

What is neuropraxia?

A

Temporary failure of nerve conduction without structural changes; due to blunt injury; compression; or ischemia. Recovery in 3-6 weeks.

243
Q

What is axonotmesis?

A

Disruption of the axon and myelin sheath with preservation of connective tissue fragments. Regeneration is spontaneous and of good quality; recovery takes months.

244
Q

What is neurotmesis?

A

Partial or complete severance of a nerve with disruption of the axon; myelin sheath; and connective tissue elements. Recovery is uncertain.

245
Q

What are the clinical features of traumatic trigeminal neuropathy?

A

Anesthesia or hypoesthesia of the mandibular branch; mental hypoesthesia; lingual hypoesthesia.

246
Q

What is the treatment for traumatic trigeminal neuropathy?

A

Prevention with correct surgical technique; informed consent; early treatment of complications with antibiotics; anti-inflammatories (corticosteroids); vitamin B complex; and patient support during recovery.

247
Q

What are the clinical features of trigeminal neuropathy caused by tumors?

A

Gradual increase in sensory deficit; associated motor and neurological problems; may indicate tumor or metastases; sign of severity and poor prognosis.

248
Q

What is malignant mental neuropathy?

A

Also known as numb chin syndrome; can be associated with non-Hodgkin lymphoma; breast and prostate cancer; multiple myeloma; leukemia; sarcomas.

249
Q

What are collagen diseases that can cause trigeminal neuropathy?

A

Polyneuropathies with sensory predominance; dysesthesias; preserved motor function and corneal reflex; associated with multiple sclerosis; Sjögren syndrome; lupus erythematosus; arthritis.

250
Q

What are the clinical features of benign trigeminal neuropathy?

A

Gradual appearance of anesthesia or paresthesia; often disappearing spontaneously in 50% of cases; no pathological background or systemic diseases.

251
Q

What are the causes of trigeminal neuropathy due to infections?

A

Odontogenic infections; third molar teeth; maxillary sinusitis; periapical lesions; viruses like herpes simplex and varicella zoster.

252
Q

What are other causes of trigeminal neuropathy?

A

Diabetic polyneuropathy; amyloidosis; sarcoidosis; secondary to masseter muscle hypertrophy; muscle contracture (pterygoids); drug neurotoxicity or antineoplastic chemotherapy.

253
Q

How is trigeminal neuropathy diagnosed?

A

Clinical examination to exclude tumors or systemic pathology; blood analysis; imaging tests; peripheral nerve conduction studies; evoked potentials; electromyography; spinal fluid study.

254
Q

What are the complementary tests used in the diagnosis of trigeminal neuropathy?

A

Blood analysis; orthopantomography; CT scan; MRI; peripheral nerve conduction studies; evoked potentials; electromyography; spinal fluid study.

255
Q

What is orofacial palsy?

A

Orofacial palsy includes facial palsy (VII cranial nerve) and hypoglossal palsy (XII cranial nerve).

256
Q

What are the functions of the facial nerve (VII)?

A

Motor: facial expression muscles. Sensory: taste from the anterior two-thirds of the tongue; hard and soft palate; outer ear.

257
Q

What are the etiologies of facial paralysis?

A

Upper face muscle innervation originates from both sides of the brain; lower face muscle innervation originates from the opposite side only. Cortical injury causes contralateral lower face weakness; facial nerve injury causes ipsilateral upper and lower face weakness.

258
Q

What are the clinical features of upper facial paralysis?

A

Middle of the face appears flaccid and smooth without wrinkles; enlarged palpebral split; loss of blinking; red and congested eye conjunctiva; affected eye turns upwards.

259
Q

What are the clinical features of lower facial paralysis?

A

Nasolabial fold is erased; buccal commissure drops; mouth moves towards the healthy side with lip movements.

260
Q

What are the types of idiopathic facial paralysis?

A

Idiopathic (most common; unknown etiology; possibly viral); Melkersson Rosenthal syndrome (labial edema; fissured tongue; facial paralysis); Heerfordt syndrome (sarcoidosis; parotiditis; facial palsy; uveitis); Ramsay-Hunt syndrome (herpes zoster of the geniculate ganglion).

261
Q

What is the treatment for facial paralysis?

A

Control of underlying conditions (blood pressure; glycemia); ocular protection (eye drops; creams; sunglasses); high-dose corticosteroids; antivirals (acyclovir; valacyclovir; famciclovir).

262
Q

What are the clinical features of hypoglossal paralysis?

A

Peripheral paralysis: ipsilateral tongue paralysis; dysarthria; difficulty in swallowing and mobility. Central paralysis: contralateral paralysis; speech disturbances; tongue curves away from the side of damage.

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