Chapter 1 to 13 OMII Flashcards
Révisions Noémie (262 cards)
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.
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.
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.
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.
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.
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.
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.
8
Q
How to manage osteomyelitis?
A
Antibiotic treatment (amoxicillin-clavulanic acid + fluocinolone); surgical drainage of pus; surgical debridement (sequestrectomy) in chronic phases.
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.
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.
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.
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.
13
Q
What is osteochemonecrosis?
A
A complication of bisphosphonate usage; characterized by transmucosal exposure of necrotic bone; often followed by infection and pain.
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.
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.
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.
17
Q
How to diagnose odontogenic maxillary sinusitis?
A
Clinical features; radiographic findings (water projection); CT to show odontogenic origin; sinus puncture.
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.
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.
20
Q
What is the classification of OT according to WHO?
A
- Benign: Tumour of odontogenic epithelium; Mixed odontogenic tumour; Tumour of odontogenic ectomesenchyma. 2. Malignant: Odontogenic carcinoma; Odontogenic sarcoma.
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.
22
Q
What are the clinical features of ameloblastoma?
A
Slow growth; asymptomatic bone expansion deformity; hard swelling; tooth mobility.
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.
24
Q
How to manage ameloblastoma?
A
Wide excision; 20% recurrence rate.
25
What is a calcifying epithelial odontogenic tumour (Pindborg tumour)?
A rare OT (1%); occurs in ages 30-50 with no sex predilection; 6% are extraosseous; commonly found in the mandible; posterior area.
26
What are the clinical features of a calcifying epithelial odontogenic tumour?
Painless slow-growing swelling.
27
What are the radiographic features of a calcifying epithelial odontogenic tumour?
Lucent area with well or poorly defined multilocular radiopacities within the lesion.
28
How to manage a calcifying epithelial odontogenic tumour?
Total resection of the lesion; 20% recurrence rate; 15% for clear cell variant.
29
What is an adenomatoid odontogenic tumour?
A rare OT (3%); occurs in ages 10-20 with female predilection; considered a hamartoma.
30
What are the clinical features of an adenomatoid odontogenic tumour?
Asymptomatic slow-growing mass; 75% associated with an impacted tooth; commonly found in the anterior area.
31
What are the radiographic features of an adenomatoid odontogenic tumour?
Well-defined radiolucency with a sclerotic margin.
32
How to manage an adenomatoid odontogenic tumour?
Surgical removal with no recurrences.
33
What is a keratocystic odontogenic tumour?
A tumour affecting young adults (20-30 years); male predisposition; commonly found in the posterior mandible.
34
What are the clinical features of a keratocystic odontogenic tumour?
Slow growth; cortical expansion; tooth displacement; associated with Gorlin Goltz Syndrome (keratocysts; bone alterations; basal cell carcinomas).
35
What are the radiographic features of a keratocystic odontogenic tumour?
Unilocular or multilocular radiolucency; cortical expansion; tooth displacement; no root resorption except for third molars.
36
How to manage a keratocystic odontogenic tumour?
Surgical excision with curettage of the underlying bone; use of chemical products like Carney solution; marsupialization for large lesions; high recurrence rate.
37
What is an osteoma?
A benign osteogenic lesion characterized by excessive and persistent proliferation of bone with slow growth.
38
What are the clinical features of an osteoma?
Slow growth; painless; typically occurs in adults; often found in the mandible.
39
What are the radiographic features of an osteoma?
Well-defined radiopaque area.
40
What is Gardner Syndrome?
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.
41
What are osteoid osteoma and osteoblastoma?
Benign bony lesions closely related; differ in size and location. Osteoid osteoma is usually cortical; osteoblastoma is medullary.
42
What are the clinical features of osteoid osteoma?
Intermittent pain; intensity increases over time; nocturnal predominance; pain relieved with NSAIDs.
43
What are the radiographic features of osteoid osteoma?
Radiolucent area; well-circumscribed 'nest' < 1 cm; surrounded by reactive sclerotic bone; may contain radiopaque areas.
44
What are the clinical features of osteoblastoma?
Less intense pain without nocturnal predominance; does not respond to NSAIDs; adjacent teeth mobility.
45
What are the radiographic features of osteoblastoma?
Osteolytic area with calcified material inside; > 2 cm; may expand or erode cortices.
46
What is an osteochondroma?
A benign tumor characterized by the formation of mature cartilage; typically occurs in tubular bones and is rare in the jaw.
47
What are the clinical features of an osteochondroma?
Painless slow-growing tumor; may cause dental mobility.
48
What are the radiographic features of an osteochondroma?
Radiolucent irregular areas.
49
What is an osteosarcoma?
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.
50
What are the clinical features of an osteosarcoma?
Rapidly growing swelling; painful; anesthesia or paresthesia; exfoliation of teeth; pathological fractures.
51
What are the radiographic features of an osteosarcoma?
Destructive bone lesion; 'sunray appearance;' symmetrical widening of the periodontal ligament.
52
What is a chondrosarcoma?
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).
53
What are the clinical features of a chondrosarcoma?
Rapidly growing tumor; later metastases.
54
What are the radiographic features of a chondrosarcoma?
Poorly defined radiolucency.
55
What is a peripheral giant cell granuloma?
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.
56
What are the clinical features of a peripheral giant cell granuloma?
Broad-based; sessile; purplish-red elevation of the mucosa; usually ≥ 1cm in size.
57
What are the radiographic features of a peripheral giant cell granuloma?
Non-specific radiolucent area; resorption of the alveolar crest; widening of the periodontal space.
58
What is a central giant cell granuloma?
A benign tumour of osteoclastic origin; not unique to the jaws or odontogenic; more common in women aged 10-30.
59
What are the clinical features of a central giant cell granuloma?
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.
60
What are the radiographic features of a central giant cell granuloma?
Well-defined; sometimes multilocular radiolucent area; crossed midline; thin cortices; displaced teeth; resorbed roots.
61
What is an aneurysmal bone cyst?
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.
62
What are the clinical features of an aneurysmal bone cyst?
Painful swelling.
63
What are the radiographic features of an aneurysmal bone cyst?
Multilocular radiolucency; cortical expansion.
64
What is hyperparathyroidism (Brown tumour)?
Resulting from overproduction of parathyroid hormone; characterized by increased calcium blood levels; commonly affects middle-aged individuals.
65
What is cherubism?
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%).
66
What are the clinical features of cherubism?
Symmetrical mandibular swellings (chubby face) beginning from ages 2 to 7; maxillary involvement causing eyes to turn upwards.
67
What are the radiographic features of cherubism?
Multilocular cysts; reduced thickness of bony cortices; diffuse rarefaction in the maxilla.
68
What is an ossifying fibroma?
A slow-growing neoplasm well-circumscribed; constituted by cellular fibrous tissue containing calcified centers resembling bone or cement.
69
What are the clinical features of an ossifying fibroma?
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.
70
What are the radiographic features of an ossifying fibroma?
Initial phase: well-circumscribed unilocular radiolucent area; Intermediate phase: radiolucent-radiopaque areas; Last phase: radiopaque.
71
What is fibrous dysplasia?
Bone replacement by fibrous tissue of unknown etiology; equally affects males and females; can be monostotic (one bone) or polyostotic (many bones).
72
What are the clinical features of fibrous dysplasia?
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.
73
What is Paget’s disease of bone?
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.
74
What are the etiological factors of Paget’s disease?
Unknown etiology; potentially viral; with genetic susceptibility (mutation P3921-P62).
75
What are the clinical features of Paget’s disease?
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.
76
What are the radiographic features of Paget’s disease?
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.
77
What are the histological features of Paget’s disease?
Bone resorption and repair with osteoclastic resorption and fibrovascular proliferation. Osteoblasts lay down new bone within a vascular stroma.
78
What are the chemical findings in Paget’s disease?
Increased levels of alkaline phosphatase; hydroxyproline; and hypercalcemia.
79
What is the prognosis of Paget’s disease?
Typically active for 3-5 years before becoming static; can cause oral complications like problems with dentures; bleeding; and bone infections.
80
How is Paget’s disease treated?
Oral bisphosphonates are commonly used.
81
What is Langerhans cell histiocytosis?
A disorder characterized by the proliferation of Langerhans cells; with 10% oral involvement; mostly in the mandible (73%).
82
What are the forms of Langerhans cell histiocytosis?
1. Solitary eosinophilic granuloma; 2. Multifocal eosinophilic granuloma; 3. Letterer-Siwe disease.
83
What are the clinical features of solitary eosinophilic granuloma?
Affects adults; causes destruction; pain; and swelling of a bone; gross periodontal destruction; root exposure; and in 10% of patients; loosened teeth.
84
What are the radiographic features of solitary eosinophilic granuloma?
Well-defined round area of radiolucency; commonly in alveolar ridges and mandible; teeth appear floating in air.
85
What are the clinical features of multifocal eosinophilic granuloma?
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).
86
What are the clinical features of Letterer-Siwe disease?
Affects infants and young children; involving bones and soft tissues. Symptoms include lymphadenopathy; splenomegaly; fever; anemia; thrombocytopenia; infections; and rashes.
87
What are the radiographic features of Langerhans cell histiocytosis?
Bone lesions similar to those in Langerhans cell histiocytosis.
88
What is the prognosis of Langerhans cell histiocytosis?
Isolated lesions may regress spontaneously; widespread disease can be fatal with a mortality rate of 15-50%.
89
How is Langerhans cell histiocytosis diagnosed?
Diagnosis is confirmed through biopsy and immunohistochemistry showing Langerhans cells; protein S100; and CD1.
90
How is Langerhans cell histiocytosis treated?
Treatment options include curettage; intra-lesional corticosteroid injections; and irradiation of active bone lesions.
91
What is Paget’s disease of bone?
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.
92
What are the etiological factors of Paget’s disease?
Unknown etiology; potentially viral; with genetic susceptibility (mutation P3921-P62).
93
What are the clinical features of Paget’s disease?
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.
94
What are the radiographic features of Paget’s disease?
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.
95
What are the histological features of Paget’s disease?
Bone resorption and repair with osteoclastic resorption and fibrovascular proliferation. Osteoblasts lay down new bone within a vascular stroma.
96
What are the chemical findings in Paget’s disease?
Increased levels of alkaline phosphatase; hydroxyproline; and hypercalcemia.
97
What is the prognosis of Paget’s disease?
Typically active for 3-5 years before becoming static; can cause oral complications like problems with dentures; bleeding; and bone infections.
98
How is Paget’s disease treated?
Oral bisphosphonates are commonly used.
99
What is Langerhans cell histiocytosis?
A disorder characterized by the proliferation of Langerhans cells; with 10% oral involvement; mostly in the mandible (73%).
100
What are the forms of Langerhans cell histiocytosis?
1. Solitary eosinophilic granuloma; 2. Multifocal eosinophilic granuloma; 3. Letterer-Siwe disease.
101
What are the clinical features of solitary eosinophilic granuloma?
Affects adults; causes destruction; pain; and swelling of a bone; gross periodontal destruction; root exposure; and in 10% of patients; loosened teeth.
102
What are the radiographic features of solitary eosinophilic granuloma?
Well-defined round area of radiolucency; commonly in alveolar ridges and mandible; teeth appear floating in air.
103
What are the clinical features of multifocal eosinophilic granuloma?
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).
104
What are the clinical features of Letterer-Siwe disease?
Affects infants and young children; involving bones and soft tissues. Symptoms include lymphadenopathy; splenomegaly; fever; anemia; thrombocytopenia; infections; and rashes.
105
What are the radiographic features of Langerhans cell histiocytosis?
Bone lesions similar to those in Langerhans cell histiocytosis.
106
What is the prognosis of Langerhans cell histiocytosis?
Isolated lesions may regress spontaneously; widespread disease can be fatal with a mortality rate of 15-50%.
107
How is Langerhans cell histiocytosis diagnosed?
Diagnosis is confirmed through biopsy and immunohistochemistry showing Langerhans cells; protein S100; and CD1.
108
How is Langerhans cell histiocytosis treated?
Treatment options include curettage; intra-lesional corticosteroid injections; and irradiation of active bone lesions.
109
What is sialadenitis?
Non-neoplastic swelling of salivary glands due to bacterial; viral; ionising radiation; obstructive; or immunological causes; commonly affecting the parotid and submandibular glands.
110
What are the modifiable risk factors for sialadenitis?
Dehydration; recent surgery and anesthesia; malnutrition; medications (e.g.; antihistamines; diuretics; tricyclic antidepressants); sialolithiasis; oral infections.
111
What are the non-modifiable risk factors for sialadenitis?
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
What are the clinical features of viral sialadenitis caused by mumps?
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
What are the clinical features of HIV;AIDS-associated sialadenitis?
Diffuse enlargement of the salivary glands at any stage of HIV infection; characterized by non-tender persistent swelling; decreased salivary flow.
114
What are the clinical features of acute bacterial sialadenitis?
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
What are the treatment options for acute bacterial sialadenitis?
Immediate IV amoxicillin-clavulanic acid every 6 hours; surgical decompression by external drainage in severe or refractory cases; or with an obvious abscess.
116
What are the clinical features of recurrent bacterial sialadenitis?
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
What are the diagnostic methods for recurrent bacterial sialadenitis?
Clinical manifestations; repeated episodes of swelling with few symptoms; sialography showing rosary or birdshot images; MRI.
118
What are the treatment options for recurrent bacterial sialadenitis?
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
What is obstructive sialadenitis (sialolithiasis)?
The most frequent pathology of the salivary gland caused by calculus (sialolith) or other factors like congenital malformations; inflammation; or autoimmune alterations.
120
What are the clinical features of obstructive sialadenitis?
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
What are the diagnostic methods for obstructive sialadenitis?
Palpation if superficial; occlusal radiography if calcified; sialography to show interruption of contrast passage; echographs; CT; MRI for acute sialadenitis.
122
What are the treatment options for obstructive sialadenitis?
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
What is radiation sialadenitis?
Inflammation of salivary glands due to external irradiation or radiodine therapy; leading to atrophy and transient or permanent oral dryness.
124
What are the clinical features of radiation sialadenitis?
Xerostomia with hyposialia; burning of the tongue; frequently combined with hypogeusia or ageusia; some recovery over years; but many patients experience persistent complaints.
125
What are the treatment options for radiation sialadenitis?
Treatment of associated symptoms; preventive measures to reduce risk of complications; pilocarpine (Salagen) 5mg 3 times a day for hyposialia.
126
What is necrotizing sialometaplasia?
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
What is sialadenosis (sialosis)?
Enlargement of the salivary glands (parotid); characterized by bilateral; non-inflammatory; non-neoplastic; soft; symmetrical; painless; and persistent swelling.
128
What are the conditions associated with sialadenosis?
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
What are the clinical features of sialadenosis?
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
How is sialadenosis diagnosed?
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
What are the treatment options for sialadenosis?
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
What is Sjögren syndrome?
A chronic systemic autoimmune disease affecting exocrine glands; characterized by lymphocytic inflammatory infiltrate that destroys glands leading to xerostomia and xerophthalmia.
133
What are the clinical forms of Sjögren syndrome?
Primary SS: keratoconjunctivitis sicca and hyposialia. Secondary SS: presence of connective tissue disease (rheumatoid arthritis; systemic lupus erythematosus; myositis; systemic sclerosis).
134
What are the aetiopathogenesis factors for Sjögren syndrome?
Multifactorial and complex; involving endocrine and genetic factors; certain viruses (Cytomegalovirus; Epstein Barr; Herpes); and alterations in cell apoptosis regulation.
135
What are the clinical features of Sjögren syndrome?
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
What are the clinical signs of Sjögren syndrome?
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
What are the extra glandular symptoms of Sjögren syndrome?
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
What is the most serious complication of Sjögren syndrome?
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
How is Sjögren syndrome diagnosed?
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
What is the ACR-EULAR classification criteria for primary Sjögren’s syndrome?
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
What are the exclusion criteria for Sjögren syndrome diagnosis?
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
What are the complementary diagnostic techniques for Sjögren syndrome?
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
What are the treatment options for xerophthalmia in Sjögren syndrome?
Xerophthalmia treatment includes artificial tears; antibiotic eye drops for conjunctivitis; and pilocarpine (Salagen) 5mg three times a day.
144
What are the treatment options for xerostomia in Sjögren syndrome?
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
What is a mucocele?
Cystic formations containing mucin; primarily from minor salivary glands and the sublingual gland; caused by mucous escape or retention.
146
What are the aetiologies of mucoceles?
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
What are the clinical features of mucoceles?
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
How are mucoceles diagnosed?
Clinical diagnosis; fine-needle aspiration (FNA); CT;MR; excisional biopsy.
149
What is the treatment for mucoceles?
Excision of the mucocele and the injured minor salivary gland; ensuring complete removal to prevent recurrence.
150
What is a ranula?
A cyst of salivary retention exclusively in the sublingual gland.
151
What are the aetiologies of ranulas?
Malformation of the duct system; trauma; infection.
152
What are the clinical features of ranulas?
Asymptomatic swelling with progressive growth; fluctuates in size; located on the floor of the mouth; may cross the midline; can burst releasing saliva.
153
How are ranulas diagnosed?
Clinical diagnosis; FNA; CT;MR; excisional biopsy.
154
What is the treatment for ranulas?
Surgical excision.
155
What are the general features of salivary gland tumours?
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
What are the clinical features of benign salivary gland tumours?
Slow-growing mass; not fixed to surrounding tissues; asymptomatic; not ulcerated.
157
What are the clinical features of malignant salivary gland tumours?
Fast-growing mass; fixed to skin and surrounding tissues; hard consistency; painful; may be ulcerated.
158
What is the TNM staging system for salivary gland tumours?
TNM system: Tumour (T) size and location; Node (N) lymph node involvement; Metastasis (M) spread to other body parts.
159
How are salivary gland tumours diagnosed?
Medical record; clinical examination (size; consistency; skin and mucosa color); imaging tests (CT; MRI; orthopantomography; echography; scintigraphy; sialography); histopathology (FNA; intra-operatory biopsy).
160
What are the treatment options for salivary gland tumours?
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
What is the WHO classification of salivary gland tumours (2005)?
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
What are the characteristics of pleomorphic adenoma?
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
What are the chief complaints in neuromuscular examination in dentistry?
Pain; decrease or loss of sensitivity; paralysis.
164
What are the key aspects of the clinical examination in neuromuscular dentistry?
Intraoral examination (lips; cheeks; palate; tongue; floor of the mouth; gums; teeth; tonsils; pharynx); application of stimuli; occlusion assessment.
165
What stimuli are used in neuromuscular examination?
Thermal; chemical; mechanical; or electrical stimuli; and percussion of teeth.
166
What is examined in the temporomandibular joint (TMJ) clinical examination?
Range of opening; articular noises; deviations on opening or closing; palpation for clicks or crepitus.
167
What are the signs of TMJ issues during palpation?
Palpation for clicks or crepitus; both sides at the same time; during rest and movement.
168
How is posterior TMJ palpation performed?
With the little finger placed in the external auditory meatus; applying pressure forwards.
169
What is the significance of auscultation in TMJ examination?
Auscultation with a stethoscope placed in the preauricular area to detect joint sounds.
170
What are the types of noises associated with TMJ disorders?
Clicks indicate disc displacement; crepitus indicates osteoarthrosis of the TMJ.
171
What muscles are included in the masticatory muscles examination?
Masseter; temporalis; medial pterygoid; lateral pterygoid; digastric; sternocleidomastoid.
172
How is sensitivity to muscle palpation assessed?
Sensitivity to muscle palpation is assessed bilaterally in movement and rest; starting with muscle insertions.
173
What are the functions of the masseter muscle?
Elevates the mandible; retracts the mandible; and performs lateral movements.
174
What are the functions of the temporalis muscle?
Involved in crushing food.
175
What are the roles of the internal and external pterygoid muscles?
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
What are the signs of masticatory muscle pain?
Sensitivity to muscle palpation; pain during bilateral palpation in movement and rest.
177
Which cranial nerves are tested in neuromuscular examination?
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
What are the sensory and motor functions of the trigeminal nerve (V)?
Sensory: face sensitivity; motor: mastication.
179
How is the corneal reflex tested?
By touching the cornea with a cotton swab while the patient looks to the side; eliciting an involuntary blink.
180
How is the motor function of the trigeminal nerve assessed?
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
What are the functions of the facial nerve (VII)?
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
How is the sensory function of the facial nerve tested?
Taste from the anterior two-thirds of the tongue; hard and soft palates.
183
How is the motor function of the facial nerve tested?
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
What are the sensory and motor functions of the glossopharyngeal nerve (IX)?
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
What are the sensory and motor functions of the vagus nerve (X)?
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
How is the motor function of the spinal accessory nerve (XI) tested?
By assessing swallowing; head and neck movement; and movement of the upper shoulders.
187
What are the motor functions of the hypoglossal nerve (XII)?
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
What is Burning Mouth Syndrome (BMS)?
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
What are the primary characteristics of BMS?
Bilateral burning or stinging in the oral mucosa; continuous for at least 3 months; no clinical lesions; improves with food and drink.
190
What is the incidence of BMS?
0.7-2.6% of the population.
191
Which demographic is most affected by BMS?
People aged 50-70; with an 8:1 female to male ratio.
192
What are the etiological factors of idiopathic BMS?
Idiopathic BMS has no known cause; often linked to neuropathic pain due to peripheral or central receptor dysfunction.
193
What is the neuropathic component of BMS?
Involves significant loss of epithelial and subepithelial nerve fibers; and alteration of nervous impulses in the trigeminal system.
194
What are the etiological factors of secondary BMS?
Local factors; systemic problems; and psychogenic causes.
195
What local factors contribute to secondary BMS?
Tongue thrusting; restricted tongue space from poor denture construction.
196
What systemic problems are associated with secondary BMS?
Haematological deficiency states; diabetes; mucosal diseases.
197
What psychogenic causes are linked to BMS?
Anxiety; accounting for 20% of cases.
198
Which areas are most frequently affected by BMS?
Tongue; palate; lips; lower alveolus; usually bilateral.
199
What are the clinical features of BMS?
Bilateral; no clinical signs of disease; relief with eating and drinking; increases as the day progresses.
200
What are the common locations for BMS symptoms?
Multicentric: tongue; lips; palate; gums.
201
What are the signs and symptoms associated with BMS?
Xerostomia; taste alterations; atypical dental pain; continuous movement of the tongue and lips.
202
How is BMS diagnosed?
Absence of objective signs that justify the symptoms; sialometry; blood analysis for secondary BMS; allergy tests.
203
What objective signs need to be absent for a BMS diagnosis?
No objective signs like glossitis; lichen planus; candidiasis; or xerostomia.
204
What tests are undertaken to exclude systemic diseases in BMS diagnosis?
Laboratory tests to exclude systemic diseases.
205
What are the primary steps in managing BMS?
Informing the patient about the condition and its management.
206
What local drug treatments are used for BMS?
Local treatments include clonazepam (Rivotril); capsaicin combined with lidocaine; benzodiazepines.
207
What systemic drug treatments are used for BMS?
Systemic treatments include clonazepam; antidepressants; benzodiazepines; gabapentin; alpha-lipoic acid.
208
What is the role of clonazepam in BMS treatment?
Clonazepam is used for its calming effect and to reduce nerve-related pain.
209
How does capsaicin help in BMS treatment?
Capsaicin is used for its pain relief properties by desensitizing sensory receptors.
210
What are the benefits of alpha-lipoic acid in BMS management?
Alpha-lipoic acid is an antioxidant that helps in reducing nerve pain.
211
What is the importance of informing the patient about BMS?
It is important to inform the patient about the nature of BMS; its chronic course; and the treatment options available to manage symptoms.
212
Why is it necessary to exclude conditions like glossitis; lichen planus; and candidiasis in BMS diagnosis?
These conditions need to be excluded as they can cause similar symptoms to BMS and require different treatments.
213
What are the primary characteristics of BMS?
Bilateral burning or stinging in the oral mucosa; continuous for at least 3 months; no clinical lesions; improves with food and drink.
214
What is the incidence of BMS?
0.7-2.6% of the population.
215
Which demographic is most affected by BMS?
People aged 50-70; with an 8:1 female to male ratio.
216
What are the etiological factors of idiopathic BMS?
Idiopathic BMS has no known cause; often linked to neuropathic pain due to peripheral or central receptor dysfunction.
217
What is the neuropathic component of BMS?
Involves significant loss of epithelial and subepithelial nerve fibers; and alteration of nervous impulses in the trigeminal system.
218
What are the etiological factors of secondary BMS?
Local factors; systemic problems; and psychogenic causes.
219
What local factors contribute to secondary BMS?
Tongue thrusting; restricted tongue space from poor denture construction.
220
What systemic problems are associated with secondary BMS?
Haematological deficiency states; diabetes; mucosal diseases.
221
What psychogenic causes are linked to BMS?
Anxiety; accounting for 20% of cases.
222
Which areas are most frequently affected by BMS?
Tongue; palate; lips; lower alveolus; usually bilateral.
223
What are the clinical features of BMS?
Bilateral; no clinical signs of disease; relief with eating and drinking; increases as the day progresses.
224
What are the common locations for BMS symptoms?
Multicentric: tongue; lips; palate; gums.
225
What are the signs and symptoms associated with BMS?
Xerostomia; taste alterations; atypical dental pain; continuous movement of the tongue and lips.
226
How is BMS diagnosed?
Absence of objective signs that justify the symptoms; sialometry; blood analysis for secondary BMS; allergy tests.
227
What objective signs need to be absent for a BMS diagnosis?
No objective signs like glossitis; lichen planus; candidiasis; or xerostomia.
228
What tests are undertaken to exclude systemic diseases in BMS diagnosis?
Laboratory tests to exclude systemic diseases.
229
What are the primary steps in managing BMS?
Informing the patient about the condition and its management.
230
What local drug treatments are used for BMS?
Local treatments include clonazepam (Rivotril); capsaicin combined with lidocaine; benzodiazepines.
231
What systemic drug treatments are used for BMS?
Systemic treatments include clonazepam; antidepressants; benzodiazepines; gabapentin; alpha-lipoic acid.
232
What is the role of clonazepam in BMS treatment?
Clonazepam is used for its calming effect and to reduce nerve-related pain.
233
How does capsaicin help in BMS treatment?
Capsaicin is used for its pain relief properties by desensitizing sensory receptors.
234
What are the benefits of alpha-lipoic acid in BMS management?
Alpha-lipoic acid is an antioxidant that helps in reducing nerve pain.
235
What is the importance of informing the patient about BMS?
It is important to inform the patient about the nature of BMS; its chronic course; and the treatment options available to manage symptoms.
236
Why is it necessary to exclude conditions like glossitis; lichen planus; and candidiasis in BMS diagnosis?
These conditions need to be excluded as they can cause similar symptoms to BMS and require different treatments.
237
What is the primary treatment goal for BMS?
The primary treatment goal for BMS is to manage symptoms and improve the patient's quality of life.
238
What are trigeminal neuropathies?
Disorders of sensation in the area of innervation of the trigeminal nerve.
239
What are the types of sensation disorders in trigeminal neuropathies?
Partial sensibility loss (hypoesthesia); total sensibility loss (anesthesia); abnormal sensations (paresthesia;dysesthesia).
240
What are the methods used in the clinical examination of the trigeminal nerve?
Light touch using a cotton wisp or tissue paper; pain using a needle.
241
What are the etiopathogenic factors of trigeminal neuropathies?
Traumatism; tumors; collagen diseases; benign trigeminal neuropathy; infections; other causes.
242
What is neuropraxia?
Temporary failure of nerve conduction without structural changes; due to blunt injury; compression; or ischemia. Recovery in 3-6 weeks.
243
What is axonotmesis?
Disruption of the axon and myelin sheath with preservation of connective tissue fragments. Regeneration is spontaneous and of good quality; recovery takes months.
244
What is neurotmesis?
Partial or complete severance of a nerve with disruption of the axon; myelin sheath; and connective tissue elements. Recovery is uncertain.
245
What are the clinical features of traumatic trigeminal neuropathy?
Anesthesia or hypoesthesia of the mandibular branch; mental hypoesthesia; lingual hypoesthesia.
246
What is the treatment for traumatic trigeminal neuropathy?
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
What are the clinical features of trigeminal neuropathy caused by tumors?
Gradual increase in sensory deficit; associated motor and neurological problems; may indicate tumor or metastases; sign of severity and poor prognosis.
248
What is malignant mental neuropathy?
Also known as numb chin syndrome; can be associated with non-Hodgkin lymphoma; breast and prostate cancer; multiple myeloma; leukemia; sarcomas.
249
What are collagen diseases that can cause trigeminal neuropathy?
Polyneuropathies with sensory predominance; dysesthesias; preserved motor function and corneal reflex; associated with multiple sclerosis; Sjögren syndrome; lupus erythematosus; arthritis.
250
What are the clinical features of benign trigeminal neuropathy?
Gradual appearance of anesthesia or paresthesia; often disappearing spontaneously in 50% of cases; no pathological background or systemic diseases.
251
What are the causes of trigeminal neuropathy due to infections?
Odontogenic infections; third molar teeth; maxillary sinusitis; periapical lesions; viruses like herpes simplex and varicella zoster.
252
What are other causes of trigeminal neuropathy?
Diabetic polyneuropathy; amyloidosis; sarcoidosis; secondary to masseter muscle hypertrophy; muscle contracture (pterygoids); drug neurotoxicity or antineoplastic chemotherapy.
253
How is trigeminal neuropathy diagnosed?
Clinical examination to exclude tumors or systemic pathology; blood analysis; imaging tests; peripheral nerve conduction studies; evoked potentials; electromyography; spinal fluid study.
254
What are the complementary tests used in the diagnosis of trigeminal neuropathy?
Blood analysis; orthopantomography; CT scan; MRI; peripheral nerve conduction studies; evoked potentials; electromyography; spinal fluid study.
255
What is orofacial palsy?
Orofacial palsy includes facial palsy (VII cranial nerve) and hypoglossal palsy (XII cranial nerve).
256
What are the functions of the facial nerve (VII)?
Motor: facial expression muscles. Sensory: taste from the anterior two-thirds of the tongue; hard and soft palate; outer ear.
257
What are the etiologies of facial paralysis?
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
What are the clinical features of upper facial paralysis?
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
What are the clinical features of lower facial paralysis?
Nasolabial fold is erased; buccal commissure drops; mouth moves towards the healthy side with lip movements.
260
What are the types of idiopathic facial paralysis?
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
What is the treatment for facial paralysis?
Control of underlying conditions (blood pressure; glycemia); ocular protection (eye drops; creams; sunglasses); high-dose corticosteroids; antivirals (acyclovir; valacyclovir; famciclovir).
262
What are the clinical features of hypoglossal paralysis?
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.
