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Periodontology YR3 BDS > Periodontal Diseases Symposia > Flashcards

Periodontal Diseases Symposia Flashcards

1
Q

What is periodontal health?

A

Periodontal health is a state free from inflammatory disease. Absence of inflammation associated with gingivitis or periodontitis, as assessed clinically, is a prerequisite for defining periodontal health. Periodontal health can exist before disease commences but equally, periodontal health can be restored to an anatomically reduced periodontium.

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2
Q

What are the determinants for clinical periodontal health?

A

Microbiological (supra gingival and sub gingival plaque composition), environmental (smoking, medications, stress, nutrition) and host (local and systemic predisposing factors)

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3
Q

What are 4 local predisposing host factors?

A
  1. Periodontal pockets
  2. Dental Restorations
  3. Root anatomy
  4. Tooth position and crowding
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4
Q

What are 3 systemic modifying factors?

A
  1. Host immune function
  2. Systemic health
  3. Genetics
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5
Q

What are controllable factors?

A

Removal of overhangs, smoking cessation, optimal diabetes control

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6
Q

What are non-controllable factors?

A

Genetic predisposition, immune status, use of critical medications

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7
Q

What are predisposing factors?

A

Any agent or condition that contributes to the accumulation of dental plaque e.g. tooth anatomy, tooth position and restorations

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8
Q

What are modifying factors?

A

Any agent or condition that alters the way in which an individual responds to sub gingival plaque accumulation e/g. smoking, systemic conditions, meds

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9
Q

What are the 4 levels of periodontal health?

A
  1. Pristine periodontal health: total absence of clinical inflammation and physiological immune surveillance on a periodontium with normal support (no attachment/bone loss).
  2. Clinical periodontal health: characterised by absence of minimum levels of clinical inflammation in a periodontium with normal support.
  3. Periodontal disease stability: in reduced periodontium
  4. Periodontal disease remission/control in reduced periodontium
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10
Q

What is periodontal disease stability?

A

A state in which the periodontitis has been successfully treated through control of local and systemic factors resulting in: minimal BoP, optimal improvements in PPD and attachment levels, lack of progressive destruction, control of modifying factors such as reduction in daily cigarette smoking

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11
Q

What is periodontal disease remission/control?

A

A period in the course of the disease during which treatment has resulted in reduction (not total resolution) of inflammation, some improvements in PPD and attachment levels but not optimal control of local/systemic contributing factors.

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12
Q

In which pts would low disease activity be an acceptable therapeutic goal?

A

Pts with long-standing disease and/or uncontrolled contributing factors like smoking or diabetes

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13
Q

What is the main risk factor for the onset of periodontitis?

A

Gingival inflammation in response to bacterial plaque accumulation (microbial biofilms)

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14
Q

What are the clinical features common to dental-plaque induced gingival conditions?

A
  • Inflammation confined to the free and attached gingiva and does not extend beyond the mucogingival junction
  • Reversibility of the inflammation by disrupting/removing the plaque
  • Presence of high bacterial plaque burden to initiate and/or exacerbate the severity of the lesion
  • Systemic modifying factors: e.g. hormones, systemic disorders, drugs which can alter the severity of the lesion.
  • Stable (non-changing) attachment levels on a periodontium which may/may not have experienced a loss of attachment or alveolar bone
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15
Q

Common clinical features of plaque induced inflammatory gingivitis

A

Erythema, oedema, bleeding, tenderness and enlargement

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16
Q

How are plaque induced gingivitis classified?

A

A. associated with bacterial dental biofilm only
B. potential modifying factors of plaque induced gingivitis: 1. systemic conditions (Sex steroid hormones, puberty, menstrual cycle, pregnancy, oral contraceptives, hyperglycaemia, leukaemia, smoking, malnutrition) and 2. Oral factors enhancing plaque accumulation (prominent subgingival restoration margins, hyposalivation) and 3. drug influenced gingival enlargements

17
Q

What drugs are primarily associated with gingival enlargements?

A
  • Anti epileptic drugs: phenytoin, sodium valproate
  • Particular calcium-channel blocker drugs e.g. nifedipine, verapamil, diltiazem, amlodipine, felodipine
  • Immunoregulating drugs e.g. cyclosporin
  • High dose oral contraceptives
18
Q

How are non-dental biofilm induced gingival diseases classified?

A

a. genetic/developmental disorders
b. specific infections
c. inflammatory and immune conditions
d. reactive processes
e. neoplasms
f. endocrine, nutritional and metabolic diseases
g. traumatic lesions
h. gingival pigmentation

19
Q

Non-dental biofilm induced gingival diseases: specific infections - Bacterial

A

Bacterial origin: Necrotising periodontal disease caused by treponema spp., selenomonas spp., Fusobacterium spp., and prevotella intermedia in pts with specific underlying risk factors i.e poor OH, smokig, stress, poor nutrition, compromised immune status e.g. HIV
NUG + NUP + NS = all signify various stages of the same disease process = NPD

20
Q

Non-dental biofilm induced gingival diseases: specific infections - Viral

A

Viral origin: usually infect specific individuals in childhood but primary infections can occur in adult life. They may give rise to oral mucosal disease followed by periods of dormancy and sometimes reactivation

  • Coxsackie: herpangia does not involve gingiva compared to hand-foot-mouth
  • HSV-1 oral manifestations
  • VZV: primary infection causes chicken pox, secondary infections causes herpes zoster (shingles)
21
Q

Non-dental biofilm induced gingival diseases: specific infections - Fungal

A

Candidosis: most common fungal infection of the oral mucosa mainly caused by C.albicans - normal commensal organism but aso an opportunistic pathogen. Most commonly presents clinically as redness of the attached gingiva often with granular surface

22
Q

Non-dental biofilm induced gingival diseases: specific infections - Autoimmune

A

Autoimmune diseases of the skin and mucous membranes: lichen planus inflammatory reaction toward an unidentified antigen in the basal epithelium layer/basement membrane zone. Common mucocutaneous disease with recurrent manifestation on the gingiva.

  • Lesions usually bilateral, often involve the gingiva and present as desquamative gingivitis causing pain and discomfort during eating and toothbrushing
  • Tailored plaque control regime can be beneficial in reducing symptoms of gingival lichen planus and improving overall quality of life
23
Q

Non-dental biofilm induced gingival diseases: reactive processes

A

Reactive processes: epulis ‘exopytic processes originating from the gingiva’ is a non-specific term and histopathology is the basis of a more specific diagnosis. Many are reactive lesions, usually no symptoms however result as a form of exaggerated tissue response to limited local irritation/trauma. The attached gingiva is the most frequently affected location.
True epulides include:
- Fibrous epulis: exophytic, smooth surfaced pink masses of fibrous consistency attached to the gingiva.
- Pyogenic granuloma: most common and shows a preference for the gingiva accounting for 75% of all cases
- Peripheral giant cell granuloma : most prevealent reactive lesion of the oral cavity. The swelling may be sessile or pedunculated, sometimes ulcerated and the appearance may resemble pyogenic granulomas.

24
Q

Non-dental biofilm induced gingival diseases: Malignant

A

Squamous cell carcinoma - commonly occurs in edentulous areas and may also occur at sites in which teeth are present. The mobility of adjacent teeth is common and invasion of the underlying alveolar bone is apparent in approx. 50% of cases.

25
Q

Non-dental biofilm induced gingival diseases: traumatic lesions

A

Wide range of causes: self-inflicted, iatrogenic, accidental. Whether physical, chemical or thermal in nature they are among the most common in the mouth.

  • Tooth brushing-induced gingival ulceration: damage varies from superficial gingival laceration to major loss of tissue resulting in gingival recession. Pts present with good OH, cervical tooth abrasion and unaffected tips of the interdental papillae at the site of injury. The condition has been termed traumatic gingival lesions.
  • Inappropriate dental flossing may also cause gingival ulceration and inflammation primarily affecting the tip of the interdental papillae.
26
Q

What are the 3 ways in which periodontal diseases are classified?

A
  1. Necrotising periodontal diseases: NUG, NP, NS
  2. Periodontitis as a manifestation of systemic diseases
  3. Periodontitis based on stages (severity) and grade (rate or progression)
27
Q

Necrotising periodontal diseases

A
  • 3 clinical features: interdental papilla necrosis/ulceration, bleeding and pain
  • Prevalence is low but they represent the most severe biofilm-related periodontal condition leadingt to very rapid tissue destruction
  • The onset, severity, extent and progression of NPD are clearly associated with the host immune response.
  • NPD in HIV pts may be more frequent and show faster progression with higher risk of evolving into more severe lesions (NP NS) and a higher tendency for disease recurrence and poor response to therapy
  • Most adults with NPD are smokers
  • Alcohol consumption has also been associated with the physiological and psychological factors favouring nPD
  • Young people 15-34 yrs in the developed world higher risk of suffering from NPD, frequently in combination with other prediposing factors. Children are at a higher risk in developing countries and normally associated with malnutrition and other infections.
28
Q

How can periodontitis present as a manifestation of systemic diseases?

A
  1. Mostly rare diseases: papillon lefevre syndrome, leucocyte adhesion deficiency and hypophosphatasia
  2. Mostly common diseases/conditions e.g. diabetes mellitus
  3. Mainly rare conditions affecting the periodontal supporting tissues independently of dental plaque biofilm-induced inflammation e.g. SCC, Langerhans cell histiocytosis
29
Q

What term has replaced “biological width”?

A

Supracrestal attached tissues: composed on the junctional epithelium + supracrestal connective tissue attachment

30
Q

Prevalence of severe periodontitis

A

6th most prevalent disease of mankind

31
Q

Prevalence of severe forms of periodontitis

A

10% of population

32
Q

How are periodontal manifestations of systemic diseases and developmental and acquired conditions classified?

A
  1. Systemic diseases/conditions affecting periodontal supporting tissues.
  2. Other periodontal conditions: periodontal abscess, endo-perio lesions
  3. Mucogingival deformities and conditions around teeth: gingival phenotype, gingiva/soft tissue recession, lack of gingiva, decreased vestibular depth, aberrant frenum/muscle position, gingival excess, abnormal colour, condition of the exposed root surface.
  4. Traumatic occlusal forces: primary occlusal trauma, secondary occlusal trauma, orthodontic forces
  5. Prostheses and tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis: localised tooth-related factors, localised dental prostheses- related factors
33
Q

Periodontal abscess

A
  • Defined as ‘localised accumulation of pus located within the gingival wall of the periodontal pocket with an expressed periodontal breakdown occurring during a limited period of time and with easily detectable clinical symptoms.
  • PA represented approx. 7.7-14%of all dental emergencies and was ranked the 3rd most prevalent infection requiring emergency treatment after dentoalveolar abscesses and pericoronitis
  • Commonly associated with reduced drainage of a deep periodontal pocket
  • PA normally associated with deep periodontal pockets, BoP, suppuration, increased tooth mobility and pain. Bone loss is normally observed on radiographic exam
  • Antimicrobial composition similar to that of periodontitis inc. P gingivalis
  • Normally cause rapid tissue destruction which may compromise prognosis of teeth
  • May lead to tooth loss, especially if they affect teeth with previous moderate-severe attachment loss
  • Most abscesses affect periodontitis pts either untreated in PeM or those undergoing active therapy
  • Considered the main cause of tooth extraction during PeM
34
Q

Endo-perio lesions

A
  • Pathological communication between endo and perio tissues of given tooth
  • Involve both the pulp and perio tissues
  • When associated with recent traumatic/iatrogenic event e.g. root fracture/perforation the most common manifestation is an abscess accompanied by pain.
  • EPL in subjects with periodontitis EPL presents slow and chronic progression without evident symptoms
  • Common signs and symptoms: deep periodontal pockets reaching close to the apex, negative or altered response to pulp vitality tests, bone resorption in apical/furcation region, spontaneous pain or pain on palpation and percussion, purulent exudate, tooth mobility, sinus tract, crown + gingival crown alterations
  • RF: periodontitis, trauma and iatrogenic events
  • Hopeless/poor/favourable prognosis
35
Q

Mucogingival deformities and conditions around teeth: which gingival biotype has a tendency to develop the most gingival recession?

A

Thin biotype

36
Q

What are the 2 types of occlusal trauma?

A

Primary occlusal trauma and secondary occlusal trauma

37
Q

Prosthesis and tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis

A
  • Anatomic tooth factors e.g. root abnormalities and fractures, tooth relationships in the dental arch and with the opposing dentition can enhance plaque retention
  • Restoration margins within the gingival sulcus do not cause gingivitis if pts are compliant with self-performed plaque control and periodic maintenance
  • Tooth supported and/or tooth-retained restorations and their design fabrication, delivery and materials have often been associated with plaque retention and Loss of attachment
  • Restorative margins placed within the junctional epithelium and supracrestal connective tissue attachment can be associated with inflammation and potentially recession
  • Adequate Periodontal assessment and treatment, appropriate instructions and motivation in self-performed plaque control and compliance to maintenance protocols appear to be the most important factors to limit or avoid potential negative effects on the periodontium caused by fixed and removable prostheses
38
Q

How are peri-implant diseases and conditions classified?

A
  1. Peri-implant health
  2. Peri-implant mucositis
  3. Peri-implantitis
  4. Peri-implant soft and hard tissue deficiencies

Periodontology YR3 BDS (1 decks)

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