Perio :()

Question 1

What are the components of the periodontium

Answer 1

1. Gingiva
2. Periodontal ligament
3. Cementum
4. Alveolar bone

Question 2

Functions of the periodontium

Answer 2

• Attachment and support for occlusal force dissipation (shock absorption)
• Nutrition – vascularized
• Sensation – mechanoreceptors in the PDL (esp. apical 1/3) aid in proprioception of the jaws

Question 3

Features of a healthy gingiva

Answer 3

o Coral pink in colour (with varying degrees of racial pigmentation)
o Stippled with a degree of translucency
o Scalloped and knife edge margin which follows the CEJ
o Interdental papilla extends to the contact area of adjacent teeth

Question 4

Features of an unhealthy gingiva

Answer 4

o Erythematous
o Oedematous
o Receded
o Loss of distinct interdental papillae

Question 5

What is free gingiva

Question 6

What is attached gingiva

Question 7

What are the three areas of the gingival epithelium

Answer 7

Junctional epithelium at the base of the sulcus
Sulcular epithelium that lines the sulcus
Oral epithelium covering the free and attached gingiva

Question 8

What is hypercementosis

Answer 8

 Prominent generalized thickening of the cementum, with nodular enlargement of the apical third of the root
 May present with cemental spikes (thought to be caused by excessive orthodontic force)
 Radiographically, the radiolucent shadow of the PDL and radiopaque lamina dura are always seen on the outer border of an area of hypercementosis, enveloping it as it would in normal cementum

Question 9

What is it and what is its presentation - Ankylosis

Answer 9

o Fusion of the cementum and the alveolar bone with obliteration of the PDL
o Occurs in teeth with cemental resorption, suggesting it may represent a form of abnormal repair
o Ultimately leads to gradual resorption of the root and its replacement with bone tissue
o Most frequently affects the primary dentition
o May also develop after: chronic periapical inflammation, tooth replantation, and occlusal trauma
o Clinical Presentation:
 Lack of physiologic mobility (requires involvement of at least 20% of the root surface)
 Metallic percussion sound
 Infraocclusion (where ankylosis has progressed)
o Consequence of obliterated PDL
 Loss of proprioception
 Physiologic drifting and eruption can no longer occur (response of the periodontium to altered force is greatly reduced)
 Pocket formation is not possible (apical proliferation of epithelium is prevented by ankylosis)

Question 10

Blood supply of the periodontium

Answer 10

o Maxilla
 Anterior and posterior superior alveolar arteries, infraorbital artery, and the palatine artery
o Mandible
 Mandibular artery, sublingual artery, mental artery, and the buccal and facial arteries

Question 11

Perio Bacteria

Answer 11

• Aggregatibacter Actinomycetemcomitans (AA)
  o Gram –ve, anaerobic, rod
• Porphyromonas Gingivalis (PG)
  o Gram –ve, anaerobic, rod
• Tannerella Forsythia
  o Gram –ve, anaerobic, fusiform
• Treponema Denticola
  o Gram –ve, anaerobe, spirochete

Question 12

Plaque formation steps

Answer 12

1. Association
   * Through purely physical forces, bacteria associate loosely with the pellicle
2. Adhesion
   * Because they possess special surface molecules that bind to pellicle receptors, some bacteria become the primary colonizers
   * Other microorganisms adhere to the primary colonizers
3. Proliferation
   * Bacteria proliferate
4. Microcolonies
   * Many streptococci secrete protective extracellular polysaccharides
5. Biofilm Formation
   * Micro colonies form complex groups with metabolic advantages for the constituents
6. Growth Maturation
   * Begins to behave as a complex microorganism
   * Anaerobic microorganisms increase

Question 13

Pathogenesis of periodontal disease

Answer 13

1. Plaque/pathogenic microorganisms locate near periodontal tissues
   a. Release LPS and antigens
   LPS
   Complex external layer lipopolysaccharide on cell wall of gram-negative bacteria
   Acts as an endotoxin and induces immune response
   2 Immune/inflammatory host response occurs
   a. Causes
   i. Vasodilation
   ii. Increased permeability of localised blood vessels
   iii. Increased release of PMN’s (polymorphonuclear granulocytes) and antibodies to the site of
   microorganisms
   b. Release PMN’s, antibodies, cytokines, prostaglandins, MMP’s (matrix metalloproteinases)
   i. PMN’s
   Products from PMN’s antigens that exacerbate the immune response, further
   triggering more PMN’s (i.e. double-edged sword)
   ii. MMP’s
   Involved in turnover of connective tissue and extra-cellular matrix
   Inflammation results in deregulation of balance between synthesis and breakdown
   Secreted by immune cells to destroy organic matrix in CT and within bone structure
   When bacterial load increases severely, more immune cells are required, and
   macrophages release MMP’s to create space for immune cells to destroy pathogenic
   microorganisms
   iii. Cytokines
   Regulate cell proliferation and activation, inflammation and repair
   Inductors include IL-1
   a. 1/3 people have IL-1 polymorphism, resulting in over-production of this
   cytokine and thus causing more tissue damage
2. Metabolism of connective tissue and bone
   a. Leading to clinical symptoms of diseas

Question 14

PSR

Answer 14

0 Health Preventative
1 BOP = gingivitis OHI and plaque removal
2 Calculus or other plaque retentive factors OHI and scaling/root debridement
3 3.5 <PPD <5.5 = periodontitis Sextants with scores of 3 require perio charting
4 PPD > 5.5 = periodontitis Full mouth perio charting + radiographs
* Furcation defect, mobility, or recession > 3.5 mm

Question 15

How does smoking cause periodontitis

Answer 15

• Cessation cannot undo past damage, but will slow down bone and attachment loss + improve responsiveness to surgical and non-surgical therapies
  o Effects can last up to 11 years post quitting
• Effects of Smoking on the Body
  o Vascular:
   Vasoconstriction induced by nicotine  impaired healing response and decreased BOP which may inadvertently mask periodontal disease
  o Host Response:
   Suppressed immune response to periodontal pathogens
   Compromised wound healing
   ↑ MMP
  o Microbial Flora:
   Changes in subgingival environment to favour periodontal anaerobes

Question 16

Risk factors for perio

Answer 16

Smoking
Stress
Pregnancy
Medications such as phenytoin, cyclosporin and ca channel blockers
Diabetes
Immunosuppressed patients
Poor oral hygiene

Question 17

Lang and Tonetti risk assessment

Answer 17

1. BOP
   * Low = < 10%
   * Moderate = 10-25%
   * High = > 25%
2. PPD > 4 mm
   * Low = up to 4 pockets
   * High = more than 8 pockets
3. Tooth loss
   * Low = up to 4 teeth lost
   * High = more than 8 teeth lost
4. Bone level/age
   * Low = 0.25
   * Moderate = 0.5
   * High = 1.0
5. Systemic/genetic (host factors)
   * High = > 1
6. Smoking
   * Low = non-smokers and former smokers (more than 5 yrs since cessation)
   * Moderate = smoking anywhere up to 19 cigarettes a day
   * High = 20+ cigarettes a day (think more than one pack per day)

Question 18

Samet and Jotkowitz risk assessment perio

Answer 18

A. Class A = Good
* 80-100% bone support
* Can be easily maintained
B. Class B = Fair
* 50-80% bone support
* Can be well maintained with rigorous periodontal and maintenance therapy
* Vertical defects or furcations that can be periodontally treated to become easily cleansable or treated predictably with regenerative therapy
* Molars are at higher risk than single-rooted teeth
C. Class C = Questionable
* 30-50% remaining bone support
* No ongoing acute outbreaks, but maintaining cleansability is difficult
* Periodontal therapy and a thorough maintenance program will enable the tooth to be maintained for an acceptable period of time
D. Class D = Compromised
* A tooth with < 30% bone support and/or one that cannot be cleansed or maintained well and has evidence of active periodontal disease
E. Class X = Non-salvageable
* A tooth with < 30% bone support and cannot be cleansed or maintained without acute outbreaks of periodontal infection

Question 19

NUG/NUP risk factors

Answer 19

A. Local Factors:
* Smoking
* Poor OH
B. Systemic Factors:
* Stress
* Hormonal imbalance
* Nutrient deficiency
* Immunosuppression (esp. HIV)

Question 20

NUG clinical features

Answer 20

• Acute, rapid onset, destructive, usually self-limiting
• Marginal necrosis – tips of papillae are ulcerated and necrotic
• Pseudomembrane – white/yellowish slough (bacteria, salivary proteins, WBC’s, RBC’s, and necrotic tissue)
• Linear erythema
• Bleeding
• Pain
• Halitosis
• Other = excessive saliva, abnormal tooth sensation, metallic taste
• Serious = lymphadenopathy, fever, and malaise

Question 21

NUP clinical features

Answer 21

• NUP involves the attachment apparatus
• Usually seen in those that are HIV +ve, with severe malnutrition, and immunosuppression
• Signs and symptoms are similar to NUG, with the addition of:
  o Deep crater-like defects due to necrosis of PDL and alveolar bone
  o Sequestering of interdental bone

Question 22

MAnagement of NUG/NUP

Answer 22

• Debridement of infected site to reduce microbial load and remove necrotic tissue
• 400 mg Metronidazole b.i.d. for 5 days
• Minimize other factors such as poor oral hygiene, stress, smoking
• Surgical correction may be required to eliminate defects to help with oral hygiene

Question 23

Gingival abscess

Answer 23

• Acute inflammatory response to impaction of foreign body into the gingiva from the oral surface or via the gingival sulcus
• Presentation = history of pain, localized gingival swelling, and clinical appearance of shiny red gingival swelling
• Removal of foreign body will result in resolution

Question 24

Periodontal abscess (what is it and what is its clinical presentation and management)

Answer 24

What is it?
* Acute destructive process in the periodontium, not from the pulp, which results in localized collection of pus

Clinical Presentation
* Periodontitis
* Swelling, oedema, and redness of infected site
* Bleeding and suppuration with pressure or probing
* Tenderness to palpation
* Hypermobility
* Lymphadenopathy, fever and malaise (occasional)
* Vital pulp
Management
* If prognosis is not hopeless:
o Drainage through periodontal pocket by debridement
o Drainage through external incision
* If prognosis is hopeless:
o Extraction + drainage via extraction site
* If systemic signs/symptoms are present or drainage is inadequate:
o Antibiotics

Question 25

Herpes simplex virus

Answer 25

Clinical presentation
* Vesicles which can affect any part of the oral mucosa, hard palate and tongue are common
* Vesicles 2-3 mm in diameter and rupture leaving shallow painful ulcers
* Gingival margins swollen and red and lymph nodes may be swollen
* Fever and systemic upset
* Usually presents in children but sometimes in adults
* Oral lesions resolve 7-10 days
Management
* Acyclovir suspension as a rinse and swallowed will accelerate healing if used early
* Topical tetracycline suspension rinsed several times/day will relive soreness and may help healing