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Periodontics > pathology, classification > Flashcards

pathology, classification Flashcards

1
Q

Functions of each periodontal structure

A

-Gingiva= resist mechanical trauma and to defend against microorganisms.
-Periodontal ligament= tooth attachment (sharpey’s fibres from cementum and bone), withstands forces of mastication, sensory, remodelling, nutritive (highly vascular)
-Cementum= anchor for PDL
-Alveolar bone= supports the teeth

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2
Q

What are the 4 categories in the 2017 perio classification system

A
  1. Periodontal health, gingival diseases and conditions
  2. Periodontitis
  3. Other conditions affecting the periodontium
  4. Peri-implant diseases and conditions
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3
Q

What are the 6 categories in Periodontal and gingival diseases

A

Periodontal and gingival health
Biofilm-induced gingiviits
Non-biofilm induced gingivitis

Necrotising periodontal diseases
Periodontitis
Periodontitis as a manifestation of systemic disease

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4
Q

What 5 categories are in the other conditions affecting the periodontium

A

Systemic diseases affecting the periodontium
Periodontal abscesses and end-perio lesions
Mucogingival deformaties and conditions
Traumatic occlusal forces
Tooth and prosthesis related factors

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5
Q

What 4 categories in peri-implant diseases and conditions

A

Peri-implant health
Peri-implant mucositis= gingivitis with implants. No bone loss beyond initial bony remodelling
Peri-implantitis= periodontitis with implants. Bone loss
Peri-implant and hard tissue deficiencies= factors affecting tissue deficiencies at dental implants. Eg. Tooth loss prior to implant placement, mispositioned implants

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6
Q

Why alveolar mucosa is darker in colour

A

Alveolar mucosa darker in colour due to being more vascular, overlying epithelium is thinner, and non-keratanised

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7
Q

Difference between lining mucosa and masticatory mucosa (functions, sites, layers)

A

-Lining mucosa= epithelium, lamina propria, submucosa, bone.
-submucosa provides mobility and acts as cushion

Masticatory mucosa= epithelium, lamina propria, periosteum, bone. Lamina propria is more fibrous and directly attached to the periosteum of bone.
-Resists masticatory forces. middle of hard palate and gingiva

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8
Q

What type of epithelium is in the oral mucosa. What are the 4 layers of the epithelium

A

-stratified squamous epithelium
Out going in:
1. Keratinised layer
2. Granular layer
3. Prickle cell layer
4. Basal layer

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9
Q

What are the sites for orthokeratanised, parakeratanised and nonkeratanised epithelium

A

Ortho= resist against abrasion so hard palate and tongue
Para= gingiva. Resists abrasion
Non= lining mucosa

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10
Q

Role of plaque in periodontal disease. Signs of disease

A

-Pellicle on the tooth attracts early steptococci colonisers (aerobic, gram positive). As the environment changes due to poor OH or smoking, dysbiosis occurs where there is a shift in the microbial population
-Plaque builds up subgingivally, causing bridging and late colonies which are pathogenic (anaerobic, negative). Subgingivally, these cause an inflammatory response.
-Exaggerated response to infection causes gingival inflammation (heat, pain, redness, swelling, loss of function), increased sulcus depths (>3mm), vasodilation, GCF, blunting of interdental papilla.
-Progression causes periodontal tissue breakdown (protease), collagen breakdown (collegenases), mobility, loss of attachment, bone loss (osteoclasts stimulated by lipoteichoic acid), mobility

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11
Q

How calculus forms. What are sialoliths

A
  • Plaque hardens to become calculus if not removed.
  • Caused by precipitation of minerals from saliva and gingival crevicular fluid. Precipitation kills cells but the hardened surface is ideal for further plaque formation. And triggers inflammation
  • Calculus forms mostly near salivary duct openings where there is greater flow of minerals.
  • Sialoliths: calcified minerals in salivary glands and ducts - supersaturated calcium phosphate
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12
Q

Functions of saliva. what 3 enzymes are found in it

A

Functions of saliva
- Aid in digestion
- Antimicrobial effects (lysozyme, defensins)
- Forms food bolus to make food easy to swallow
- Mineralisation (statherin, PRPs)
- Moistens and lubricates the mouth to help with speech and to protect mucous membranes (mucins)
- Buffering
-prevents drying of gingiva and teeth
- Washes away debris and bacteria
- Lysozyme: breaks down peptidoglycan in cell wall, leading to cell death.
- Lactoperoxidase: converts H2O2 (a by-product of streptococci) into hypothiocyanous acid which is more toxic to all bacteria.
- Lactoferrin: binds iron and hides it making it unavailable for bacteria that need it to survive.

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13
Q

Changes that occur in pockets during disease

A
  • GCF increases (triggers infalmmtion)
  • Inflammatory mediators (cytokines)
  • Anaerobic conditions and bacteria
    -change in nutrition - no supraginigval diet sugars, now GCF proteins
  • Alkaline (anaerobes metabolise proteins (proteolytic metabolism) which releases urea and ammonia
  • increase in temperature (due to increased blood flow of inflammatory response)
  • change in oxygen-reduction metabolism
    -more pathogenic bacteria
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14
Q

What are the 3 red complex bacteria and their virulence factors and shapes

A
  1. Tannarella foryshtia: short rods. Can hide from immune system and invade epithelial cells
  2. Porphyromonas gingivalis: short rods. Fimbriae for adhesion and invasion.
    - capsule to resit phagocytosis
    - LPS to trigger inflammatory response
    - Haemagluttinins to bind to epithelial cells
    - proteases to break down proteins (collagen, fibrinogen)
  3. Treponema Denticola: spirochete. Flagellum for motility. Adhesion, degrade collagen.
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15
Q

What bridges early and late colonisers. Virulence factors

A

Fusobacterium nucleatum
-proteolytic, anaerobic.
-coaggregates to form links between early and late
-invades epithelial cells and carries other bacteria in

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16
Q

What bacteria is involved in severe perio. Facts, virulence factors, shape

A

Aggregatibacter actinomytemcomitans
- involved in severe periodontitis. Also causes endocarditis
- anaerobic, non-motile, capnophilic (CO2), haemolytic, coccobacillus
- Adhesion and invasion due to fimbriae
- LPS which triggers bone resorption
- Leukotoxin: kills WBCs
- Proteases
star shaped

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17
Q

How long it takes for full biofilm thickness. How long it takes for clinical signs to show after plaque starts to accumulate

A

24 hours to reach full thickness
Clinical signs are present within 4-5 days of undisturbed plaque accumulation and maturation

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18
Q

Local and systemic factors for gingivitis. Management

A

Local factors= plaque, calculus, overhanging restorations, tooth anatomical factors, crowding, malocclusion, appliances, oral dryness
Systemic factors =puberty, pregnancy, menstural cycle (hormones), diabetes (inflammation aggravated by poorly controlled glucose levels), meds, malnutrition, smoking
Management= OHI, brushing, scaling, removal of plaque retentive factors, potentially change meds

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19
Q

What probe is used to measure BPE scores. What measurements are marked

A

-WHO probe
0.5mm ball
first black band= 3.5-5.5mm
second black band=8.5-11.5mm

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20
Q

Other than plaque, what else can cause periodontal disease

A

genetics, infection (bacterial, viral, fungal), immunological, neoplasms (premalignant and malignant), trauma (mechanical, chemical trauma), endocrine, reactive lesions (exaggerated tissue responses), systemic disease

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21
Q

How pregnancy causes periodontal disease. How dentists should manage these patients

A

elevated oestrogen and progesterone increases vascular permeability and blood flow in gingival tissues. Makes them more sensitive and inflamed
-identify stage in pregnancy, full perio exam, educate, treatment regime, 3 monthly recall

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22
Q

What is hereditary gingival fibromatosis

A

slow progressive gingival overgrowth causing generalised gingival enlargement. Can cause diastemas, malpositioned teeth

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23
Q

What medications can cause gingival hyperplasia

A

phenytoin, cyclosporine, nifedipine, amlodipine, and vigabatrin

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24
Q

What 4 autoimmune conditions can contribute to periodontal disease/ mucocutaneous disorders

A

-Lichen planus –autoimmune disease of skin and mucous membrane. Flakey white patches surrounded by erythema.
-Pemphigus vulgaris- Intra-epithelial bullae in skin and mucous membranes. Desquamative gingivitis
-Pemphigoid- autoantibodies towards antigens of the basement membrane. Detachment of epithelium from the connective tissue. Desquamative lesions of gingiva. Intense erythematous lesions
-Lupus erythematosus: autoimmune disease attacking lots of body parts. Mucosal ulcers, burns, xerostomia, TMJ disease, perio disease, oedema etc

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25
Q

How type IV hypersensitivity reactions may cause periodontal disease

A

allergic reactions to restorative materials, toothpastes mouthwashes, meds, food, nickel, acrylic etc. This may cause erythema multiform and gingival inflammation

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26
Q

What premalignancies (2) and malignancies (3) can affect the oral cavity. Their appearance

A

-Leukoplakia (premalignant)- white lesion on oral mucosa that cannot be characterized by any other definable lesion
-Erythroplakia (pre) – red lesion

-Squamous cell carcinoma (malignant) – may mimic other oral lesions affecting the periodontium, most of which are inflammatory in nature. Redness
-Leukemia (malignant) –gingival bleeding and swelling. rapid gingival hyperplasia. Deep punched out ulcerations and necrosis on gingiva and tooth mobility
-Lymphoma (malignant) - Non-specific gingival swelling may be the first manifestation of non- Hodgkin lymphoma and may mimic a periodontal abscess or pyogenic granuloma

Cancers often have irregular borders

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27
Q

What types of bacterial infections can cause non-plaque induced gingivitis. 4 types

A

-Neisseria gonorrhoea: Ulcers of fiery red mucosa and white pseudomembrane with or without symptoms
-Treponema pallidum: Fiery red, oedematous and often painful ulcerations, asymptomatic chancres or non-ulcerated, inflamed gingivitis
-Mycobacterium tuberculosis: Nodular or papillary proliferation of inflamed gingival tissues
-Streptococcci: acute gingivitis not associated with plaque

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28
Q

What virus causes hand foot and mouth disease. Oral manifestations

A

coxsackie virus A. Usually in children. Multiple cutaneous lesions and vesicles that rupture and ulcerate. common in children. Oral lesions are bright red which later form grey vesicles.

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29
Q

What causes Primary herpetic gingivostomatitis. Oral manifestations. Transmission. Complications. Treatment

A

HSV1. Usually in children 2-5. Aggressive marginal gingivitis. formation of multiple fluid filled vesicles which burst to leave ulcers in attached gingiva and hard palate. Multiple lesions coalesce to form larger irregular ulcers. Causes erythema and bleeding. Vesicles can erupt and ooze clear yellow fluid
-transmission via direct contact with infected lesions from saliva
-could spread causing conjunctivitism encephalitis or herpetic whitlow on the fingers
-managed: chlorhexidine for plaque control. Acyclovir

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30
Q

Which virus is HHV3. Oral manifestations of primary and latent infections

A

Varicella zoster virus
– chicken pox = Small yellowish oral vesicles which rupture, along with skin rash and fever
-shingles = reactivation. Unilateral oral lesions. Vesicles coalesce to form painful ulcers. Also associated with skin lesions. Tingly sensation. In trigeminal area causes unilateral lesion on tongue via lingual branch

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31
Q

Oral manifestations of human papilloma virus

A

can cause benign oral lesion –cauliflower shaped warts. Refer to oral surgery. Virus associated with cervical and head & neck cancer

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32
Q

Oral manifestations of necrotising gingivitis and its risk factors. What bacteria is associated with it. Management

A

-acute inflammation with necrosis of interdental papilla, bleeding and pain. Halitosis. superficial infection of gingival margins with yellow-grey pseudomembranous sloughing of margin - full of dead epithelial cells, fibrin, leukocytes, erythrocytes, bacterial debris.
-associated with anaerobic fuso-spirochetal bacteria.[treponema species, fusobacterium species, prevotella intermedia]
Factors= plaque, immunocompromised, stress, poor diet/ general health/ OH, smokers, leukaemia, anaemia
-management: OHI, PMPR, risk factor management, CHX mouthwash, H2O2 mouthwash to kill anaerobes, metranizadole if systemic
-If patient doesn’t appear to have these risk factors, get in touch with GP as patient may have an immunosuppressive underlying medical condition
-usually in ages 16-30

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33
Q

What vitamin deficiency can cause gingival bleeding, ulceration and swelling.

A

vit C

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34
Q

What reactive lesions can occur due to local irritation or trauma and what they look like

A

-Fibrous epulis - an overgrowth
-pyogenic granuloma - benign overgrowth
-Peripheral giant cell granuloma/ giant cell epulis - purple/red soft tissue nodule

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35
Q

Pocket depths and BOP in health, localised gingivitis, generalised gingivitis

A

-Health= <3mm. <10% BOP
-Localised gingivits= <3mm. 10-30% BOP
-Generalised gingivitis = >3mm. >30% BOP

36
Q

What is necrotising stomatitis (aka cancrum oris/ noma) Risk factors

A

-severe inflammatory condition of the periodontium with necrosis beyond the gingiva, bone denudation through alveolar mucosa and formation of bony sequestrum (tissue detached from bone)
-severe gangrenous disease that causes rapid necrotizing destruction of soft and hard tissue of the face, including bone.
-risk factors= malnutrition, poor OH, compromised immune system (measles, malaria, HIV etc.)

37
Q

examples of a mucogingival deformities and conditions

A

-aberrant frenum = V shaped bony cleft between 2 central incisors so frenum attached too close to gingival margin so compromises brushing etc
-lack of keratinised tissue
-gingival recession

38
Q

Explain the perio classifications of traumatic occlusal forces and tooth and prosthesis-related factors

A

-Traumatic occlusal forces: eg.. High restorations could cause tooth movements. Orthodontic forces can cause bone loss
-Tooth and prosthesis-related factors: eg. Tooth anatomic factors, overhanging restorations.

39
Q

Definitions of chronic and aggressive periodontitis

A

-Chronic= Progresses slowly and bone loss reflects the age of patient. no consistent pattern to the number and types of teeth involved. localized or generalised
-Aggressive periodontitis - very severe considering the age of the patient, rapid progression usually in younger patients, associated with familial history of perio. the absence of systemic diseases. Plaque may be inconsistent with level of disease

40
Q

What factors may affect probing accuracy

A

probing force, angulation, thickness, markings accuracy, examiner experience, degree of inflammation of tissues, calculus, tooth contour, visibility

41
Q

Rough percentage of those with periodontitis, and with severe periodontitis

A

about 50% with perio
8% with severe

42
Q

What stage means for perio classification. And the classifications

A
  • looking at the worst site of bone loss. Severity of disease
    1: Early/mild= <15% bone loss or <2mm from CEJ
    2: Moderate= loss at coronal 1/3 of root
    3: Severe= mid 1/3
    4: Very severe= apical 1/3
43
Q

What grade means for perio classification. And the classifications

A

bone loss % / age. Rate of progression
A: slow rate= <0.5
B: moderate progression= 0.5-1.0
C: rapid= >1

44
Q

How to class stable, in remission, unstable periodontitis (BOP, PPDs)

A

Currently Stable= BOP<10%. PPD ≤4mm. No BOP at 4mm
Currently in remission (decreasing)= BOP ≥10%. PPD ≤4mm. No BOP at 4mm sites
Currently unstable= PPD ≥5mm or PPD ≥4mm with BOP

45
Q

How many teeth must a sextant have when recording BPE

A

at least 2. If not then include the 1 into an adjacent sextant

46
Q

Explain the codes 0-3 for tooth mobility

A

0= physiological mobility (<0.2mm) [accommodates masticatory forces]
1= 0.2 - 1.0mm horizontal
2=>1mm only horizontal
3=horizontal >1mm and vertical

Pathological= due to connective tissue attachment loss, bone loss, PDL gingiva inflammation. Irreversible.

47
Q

Explain the furcation classifications. What instrument to use

A

Class I = <3mm horizontal probing. <1/3 way through
Class II= ≥ 3mm or 2/3 way through
Class III= through and through lesion

Use Naber’s probe: it is curved and each band and gap is 3mm

48
Q

Code 0: Pocket depth, appearance, treatment

A

<3.5mm
no calculus, no BOP
no treatment

49
Q

Code 1: Pocket depth, appearance, treatment

A

<3.5mm
BOP, no calculus
OHI

50
Q

Code 2: Pocket depth, appearance, treatment

A

<3.5mm
supra or sub gingival calculus
OHI, remove plaque retentive calculus, PMPR

51
Q

Code 3: Pocket depth, appearance, treatment

A

3.5-5.5mm. Black band partially covered
Bleeding and calculus, pockets
-OHI, PMPR, x-ray (DPT), plaque score, PPDs of that sextant, RSD if required. Review in 3 months

-if pockets <4mm and no evidence of bone loss go to code 0/1/2 pathway [gingivitis]
-if pockets ≥4mm and/or evidence of bone loss continue with code 4 pathway [periodontitis]

52
Q

Code 4: Pocket depth, appearance, treatment

A

> 5.5mm (Black band covered) and/or Interdental recession
-OHI, PMPR, x-ray, plaque score, PPDs of full mouth, RSD Review in 3 months. Consider referral to specialist

53
Q

After BPE and x-ray, how to class health, localised gingivitis, generalised gingivitis, periodontitis molar-incisor pattern localised periodontitis, generalised periodontitis

A

Code 0/1/2 or 3 with no bone loss
-Health: BOP <10%
-Localised gingivitis: BOP 10-30%
-Generalised BOP: >30%

Code 3 with bone loss, or code 4
-Localised periodontitis: <30% of teeth with bone loss
-Generalised periodontitis: ≥30% of teeth with bone loss
-Molar-incisor pattern: only molars and incisors affected by bone loss

54
Q

Describe the stages of an initial, early, established and advanced periodontal lesion. Cells involved and the timings

A

-Initial lesions (24-48 hours)= localized to gingival sulcus and adjacent periodontal tissues. Local vasodilation and increased vascular permeability. Increased GCF. Neutrophils migrate into gingival sulcus via junctional and sulcular epithelium. Few lymphocytes and macrophages present in JE.
-Early lesion (4-7 days)= further increased vascularity and GCF. Lymphocytes and neutrophils are the predominant infiltrating cells. Fibroblasts degenerate. Collagen destruction to create space for the infiltrating cells. JE still at CEJ so no attachement loss at this point
-Established lesion (2-3 weeks)= further increased GCF. Dense inflammatory cell infiltrate. Neutrophils mainly and also plasma cells. Fibroblasts continue to show signs of damage. Loss of collagen. JE more leaky and thinner. Redness, swelling, bleeding, Still no loss of attachment.
-Advanced lesion= periodontal breakdown. Pockets form, micro-ulceration of pocket, loss of attachment, destruction of PDL, bone resorption, mobility, tooth loss. Migration of epithelial attachment towards the apex. Subgingival plaque formation.

55
Q

In an innate immune response, what are the functions of macrophages, and neutrophils

A

-Macrophages recognizes pathogens then releases cytokines to signal recruitment of neutrophils to initiate inflammation. They are antigen presenting cells to activate T cells. Professional Phagocytes (engulf microbes by phagocytosis at infected sites to kill them)
Scavenger cells.
-Neutrophil chemotaxis caused by cytokine signaling (produced by macrophages), and complement components. Influx causes swelling. Professional phagocytes. Contain lysozymes. Are phagocytosed by scavenger macrophages

56
Q

How are MMPs recruited and what do they do. What controls their activity

A

-Macrophages secrete cytokines which stimulate fibroblasts/ keratinocytes/ endothelial cells/ osteoclasts/neutrophils to secrete MMPs (matrix metalloproteases).
-They rearrange and degrade bone and connective tissues. Excessive cytokines and MMP causes tissue destruction
-TIMPs (tissue inhibitor metalloproteases) are produced by fibroblasts and macrophages to control MMPs. Are influenced by cytokines

57
Q

What cells secrete cytokines. Examples that are involved in bone resorption

A

neutrophils, macrophages, dendritic cells, mast cells
- proteins that lead to a cellular response, playing a key role in the immune response
-IL-1β, TNF-α and IL-6

58
Q

Role of prostaglandins in periodontitis

A

-bone resorption, neutrophil chemotaxis, vascular permeability, and dilation

59
Q

Difference between innate and adaptive response

A
  1. Innate: first line of defence. Rapid
    -Basic level of protection
    -Fixed
    -constant during exposure
    -Limited specificity (reaction to all bacteria of a species)
    -No memory
    -Neutrophils

2.Adaptive
-Slow to develop
-Highly specific and respond to wider range of pathogens
-Variable
-Improves upon exposure
-Has memory. Long-lasting protection against infection. T cells, B cells, antibodies

60
Q

What are the professional antigen presenting cells, signalling the adaptive system,

A

dendritic cells, macrophages

61
Q

What are the 5 types of CD4 T cells

A

-Th1: macrophage recruitment
-Th2: associate with allergies (mast cells etc.)
-Th17: neutrophils and AMP. Reinforce innate
-Tfh: B cells
-Treg: suppress T cells

62
Q

What are the roles of interleukins 1,2,4,8,6,12,10

A

IL-1 = inflammatory response
IL-2= T cell division and proliferation (growth stimulating factor)
IL 4= allergy cells and enhance barrier function at mucosal surfaces
IL8 = Neutrophil chemotaxis
IL6= B cell activation, by T helper cells
IL12= T cell activation
IL10- suppress T cell activity, prevent autoimmunity

63
Q

True and false periodontal pockets. Suprabony and infra bony pockets

A

-TRUE POCKETS = result from apical migration of the junctional epithelium following loss of connective tissue attachment to the root surface
-FALSE POCKETS= result from gingival enlargement with no alteration in the position of the junctional epithelium
-Suprabony pockets – JE coronal to the alveolar crest
Infrabony pockets – JE extends apically beyond the alveolar crest

64
Q

What causes BOP. Why it may not appear in smokers

A

Occurs when thin ulcerated junctional and pocket epithelia are penetrated by probe tip
-Smokers have increased vasoconstriction so might not see the bleeding we may expect

65
Q

Horizontal and vertical bone resorption

A

Horizontal loss= when the entire width of interdental bone is resorbed
-Vertical loss= the interdental bone adjacent to the root surface is more rapidly resorbed. An angular, more uneven morphology

66
Q

What causes halitosis. Why common in smokers. What test is used for diagnosis

A

-Due to plaque stagnation changes in biofilm (due to dry mouth, poor OH, smoking, plaque retentive factors)
-abscesses, tumors, tonsillitis, smelly foods, rotting food debris
-extra-oral causes: bronchitis, diabetes, kidney failure, liver disorders, trimethylaminuria
-Gram negative periodontal pathogens metabolize substrates, producing volatile sulphur compounds. Proteolytic metabolism.
-Common intra-oral sources are pockets and the posterior dorsal tongue
-smoking dries the mouth, can alter microbial population, can exacerbate post-nasal drip, contains volatile sulphur compounds
-BANA test for anaerobic proteolytic bacteria

67
Q

Probes you can use for PPDs

A

Williams probe: lines for every mm
UNC: black band at 4-5mm, 9-10mm, 14-15mm

68
Q

Gingival recession classifications (RT1-3)

A

Measured from CEJ to margin

RT1: recession with no loss of interproximal attachment. Interproximal CEJ is clinically not detectable at mesial and distal aspects of the tooth.

RT2: recession associated, with loss of interproximal attachment. Amount of interproximal attachment loss ≤ buccal attachment.

RT3: recession associated with loss of interproximal attachment. amount of attachment loss > the buccal attachment loss.

69
Q

What is clinical attachment loss (CAL) How it differs to recession

A

How far has junctional epithelium moved down the root of the tooth (from CEJ to base of pocket)
-PPD minus recession = CAL

70
Q

The steps in a full perio assessment and examination

A
  1. History and clinical observation
  2. BPE
  3. Plaque scores (then PMPR to reduce inflamed gums so accurate PPDs)
  4. Six point pocket chart (PPDs)
  5. BOP
  6. Tooth mobility
  7. Furcation
  8. Recession
    (9. Clinical attachment loss)
  9. Radiographs recommended for BPE 3 or 4s.
71
Q

What x-rays can be used for perio examination

A

-PAs gold standard
-DPT for generalised perio
-Horizontal bitewings: for early posterior bone loss
-Vertical bitewings: for severe posterior bone loss (patient needs to have tall palatal vaults)

72
Q

What should be included in a radiograph report. Specific things to report on for perio cases and for extractions

A

-patient name and DOB. Date taken
-type of radiograph. Grade A or U
-scan anatomical landmarks
-teeth present, missing, unerupted
-restorations, any overhanging
-caries
-PAP, widening of PDL
-furcation sites
-calculus
-if xtns: root morphology, relation to nerves, relation to sinus, retained root sub gingival?
-cycts, bone or sinus defects
-bone levels: localised/ generalised, which sites, vertical/ horizontal, regular/ irregular, % loss from CEj to apex, furcations at which sites

73
Q

What is an abscess. 4 types of acute periodontal abscesses. Management of abscesses

A

-Pus (neutrophils and bacteria) builds up and is walled off by a barrier due to an inflammatory response to the bacterial infection. If the pus cannot drain it forms an abscess
-gingival, periodontal, peri-coronal, endodontic-periodontal abscesses
-managed by finding the cause, remove cause (debride, irrigate, incise, drain) or antibiotics if systemic (fever, lymphadenopathy)

74
Q

Gingival abscesses: what, presentation, aetiology

A

-localized accumulation of pus in the marginal gingiva or interdental papilla (not into periodontal tissues)
-Presentation: localized swelling, perhaps suppuration, painful, TTP
-Aetiology: subgingivally impacted foreign objects (bitten nails, fish bones, toothbrush bristle etc.)

75
Q

Periodontal abscesses: what, presentation, aetiology, local risk factors. If systemic what antibiotic

A

-localized accumulation of pus in gingival wall of periodontal pocket resulting in destruction of collagen fiber attachment and loss of bone
-Presentation: localized swelling in gingiva at side of root, deep pockets, BOP, perhaps TTP, perhaps suppuration, perhaps tooth feels high in occlusion, perhaps mobility, tooth vital, bone loss
-Aetiology: due to periodontitis, reduced capacity for drainage, foreign bodies, calculus fragments from scaling dislodging.
-Local factors= change in subgingival microbiota, increase in bacterial virulence, decreased host defense, complex pocket morphology, furcation involvement or vertical defect. (Perio pathogens involved)
-500mg amoxicillin capsules 3 times per day for 5 days (broad-spectrum) OR 400mg metronidazole tablets 3 times per day for 3-5 days (for deeper anaerobic infection

76
Q

Peri-coronal abscesses: what, presentation, aetiology. management

A

-localized accumulation of pus within the overlying gingival flap surrounding the crown of an incompletely erupted tooth. Causes pericoronitis. Common at impacted wisdom tooth
-Presentation: painful red swelling at partially erupted tooth, perhaps suppuration, perhaps swelling at angle of mandible, perhaps trismus
Aetiology: accumulation of debris and anaerobic bacteria at overlying operculum
-irrigate with chlorhexidine or saline. Give syringe to patient to do at home. use metranizadole if systemic as anaerobic

77
Q

Endo-perio abscesses: what, presentation, aetiology, management

A

-localized lesions originating in periodontal and/ or pulpal tissues. Acute or chronic. Communication between the periodontal pocket and pulp
-Presentation: deep pockets, non-vital tooth, swelling of gingiva or mucosa, perhaps suppuration, perhaps TTP, perhaps mobile, radiolucency at apex, bone loss
-Aetiology: Pulpal inflammation expressed through PDL and bone to oral cavity. AND/OR Initiated from periodontal pocket to the pulp apically through lateral canals
-managemnt= drain. long term= RCT or xtn

78
Q

How necrotising periodontitis differs from necrotising gingivitis

A

-necrotising periodontitis is the same but with perio tissue destruction as it extends to PDL and bone. Management is the same. Refer to specialist as may need surgery to remove bony sequestrate
-much more rare
-usuall associated with systemic conditions (HIV, severe immunosuppression

79
Q

How smoking can cause perio

A

nicotine= vasoconstriction = reduced blood flow and reduced phagocytic activity of leukocytes. So reduced immune response and healing so tissue destruction
-Vape chemicals also reduce blood flow so increases gum disease. Also makes you more likely to smoke. But better than smoking so recommended for smokers, but not for non-smokers

80
Q

Latency definition

A

virus can re-infect the host following primary infection, by reactivating if patient is compromised. The virus infects neuronal cells and travel to nerve ganglia where they replicate and establish a latent infection. Triggers reactivate it and it travels along the neuron and develops secondary infection in the relevant dermatomes where the nerve innervates.

81
Q

What infections does HSV1 and HSV2 cause. What latent infection

A

HSV1 = causes disease above the waist. Infects epithelial cells around the mouth. Oral and pharyngeal ulceration, meningitis, encephalitis, dermatitis, conjunctivitis, gingivostomatitis, herpetic whitlow. Later reactivation causes cold sores
HSV 2= disease below the waist. Sexually transmitted. Associated with anogenital area. Painful blisters, links with cervical cancer. Latent = cold sores

82
Q

How is herpes labials caused. Symptoms

A

-cold sores. Latent infection of HSV1 and 2 due to common cold, stress, menstruation, immunosuppression.
-prodromal burning, itchy or tingling of the site of future blisters. Lesions typically appear at mucocutaneous junction of lip. Fluid-filled semi translucent blisters can enlarge which weeps. Rupture and crust over after 2-3 days. Lesions can last 12 days. Acyclovir reduces symptoms if started within 1-2 days of vesicle eruption.

don’t treat until crusted over

83
Q

What are the 4 types of oral candida infections. risk factors

A
  1. Acute Pseudomembranous candidiasis: white plaques that can be removed. due to inhalers, AIDs, elderly
  2. acute erythematous candidiasis: red inflamed tongue, loss of papilla. due to steroids or antibiotics
  3. chronic erythamtous: denture induce stomatitis
  4. chronic hyperplastic candidiasis: thickened white plaque at corner of mouth. premalignant. smoking, alcohol
84
Q

What is histoplasmosis. what is linear gingival erythema

A

-Histoplasmosis: rare systemic fungal infection. Oral symptoms rare. Often associated with AIDS
-Linear gingival erythema: erythematous line at gingival margin. Common in HIV, often associated with candida infection

85
Q

what resources to use when prescribing

A

use the BNF, SDCEP drug prescribing in dentistry, FGDP (UK) antimicrobial prescribing for GDPs, BSP Good Practioner’s Guide

86
Q

what traumatic injuries can occur to gingiva (chemical, thermal, physical)

A
  1. Traumatic chemical conditions
    Aspirin burns: due to sucking.
    Acid etch gel/ sodium hypochlorite during dental treatment.
    Hydrogen peroxide in tooth whitening
    Cocaine
  2. Thermal trauma:
    Hot food and drink
    Dental treatment (eg. Inadequate cooling of dental instruments like lack of water for cavitron)
  3. Physical/ mechanical
    -Accidental: foreign bodies, sharp food, harsh brushing, harsh flossing
    -Iatrogenic: retraction cords (used for moisture control for crowns), burs, polishing discs
    -Factitious (patients themselves): finger nails
87
Q

How much pressure to apply to probe when using WHO BPE probe

A

20-25g

Periodontics (2 decks)

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