Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
16 Cards in this Set
- Front
- Back
Question 1: state how periodontal diseases are classified.
|
- The rate of disease progress (chronic vs. aggressive)
- Lesion distribution (localized vs. generalized) - Age Group - Association with Systemic or Developmental Disorders |
|
Question 2: define
a) Localized aggressive periodontitis b) Calculus c) Chronic periodontitis |
a) Localized aggressive periodontitis
Localized (LAP), also termed juvenile periodontitis, which has onset at puberty and involves the incisors and first molars, with responses largely based on hyper-humoral (IgM, IgG, IgA) immune responses. b) Calculus Dental calculus is calcified dental plaque, composed primarily of calcium mineral salts deposited between and within the remains of formerly viable microbes. c) Chronic periodontitis Chronic periodontitis is the loss of connective tissue and alveolar bone support of the teeth that is the result of both the direct activity of pathogenic bacteria and plaque-induced inflammation. |
|
Question 3: name 3 diagnostic features of both chronic and aggressive periodontitis
|
Chronic Periodontitis
Found mostly in adults Presence of plaque and calculus - always extends into the cementum and are thicker than those associated with gingivitis. Slow to moderate progression of tissue destruction - progression can be accentuated by diabetes or host conditions such smoking. Filamentous Gram positive and Gram negative motile bacteria predominate. Aggressive periodontitis The severity of disease is not consistent with the occurrence of local factors such as plaque and calculus. The progression of tissue destruction is rapid. Genetic factors are involved Alveolar bone may be damaged significantly Not concurrent with systemic disease |
|
Question 4: describe the ecological plaque hypotheses
|
The ecological plaque hypothesis has also been proposed and postulates the following process:
Inflammatory response to plaque accumulation, Increased GCF flow provides nutrition to Gram negative anaerobes, Gram negative anaerobes suppress other species leading to a population shift. New Periodontopathic flora establishes a pathogenic consortium of microbes causing invasion and tissue destruction. |
|
Question 5: briefly describe periodontal microbe complexes
|
Studies based on the detection of 40 different species in around 15,000 plaque samples identified 5 major bacterial complexes, where bacteria are found in association in different clinical conditions and plaque environments.
|
|
Question 6: state at least 4 species associated with sub-gingival plaque
|
Porphyromonas gingivalis,
P. intermedia, Spirochetes, Tannerella forsythia |
|
Question 7: give an overview of how antibodies both promote and prevent periodontal disease.
|
Neutrophils are the major host defence
But it can destroy tissues with lysozymes Ab opsonises and promotes phagocytosis, complement, agglutination But it can also attract neutrophils to destroy tissues |
|
Question 8: describe immune complex reactions and hypersensitivity in periodontal disease.
|
Anaphylactic reaction (type I):
- IgE antibody on basophils and mast cells bind with antigens and histamine,prostaglandins and other effectors are released. - Localized, respiratory, GI, systemic, or shock. Cytotoxic reaction (type II): - Activation of complement and lysis of RBC (main Ab involved IgM). - ABO Blood groupings are based on antigens on RBC surface. - O (no) antigen, A antigen, B antigen, AB antigens. - Involves Drugs (haptens) binding to RBC and inducing Ab against them. Immune complex reaction (type III): Immune complexes are too large to be phagocytised. Instead of being removed by phagocytes, they attach to the basement membrane of blood vessels attracting neutrophils, complement proteins. Neutrohpils destroy the tissues. Cell mediated reactions (type IV, delayed hypersensitivity): - Involves T cells – Td, delayed hypersensitivity T cells via activation of memory cells, involved in skin reactions. Also called contact allergy. |
|
Question 1: Define Dentoalveolar infections.
|
Dentoalveolar infections are defined as pus-producing (pyogenic) infections associated with the teeth and supporting structures such as the periodontium (i.e. gingivae, periodontal ligament, cementum, and alveolar bone). (Lecture A).
|
|
Question 2: Name 4 factors affecting the kinds of bacteria isolated from root canal infections.
|
- Extension of caries
- Mechanical Exposure - Trauma - Association with periodontal disease |
|
Question 3: State what virulence factors are essential for opportunistic pathogens in the oral cavity to cause endodontic disease.
|
Infections of the pulp are almost always secondary to other tooth infections. The bacteria associated with pulp infections are typically endogenous oral microbes, which simply gain access to the pulp tissue (ie dental caries). These microbes do not express virulence factors such as invasins, or toxins, and it is only bacterial growth in the rich nutrient environment of the pulp that causes inflammation and damage.
Therefore, the characteristics of dental caries causing bacteria (ie adhesion to tooth surface, demineralisation of hard tissues with acidic metabolic products, formation of biofilm/plaque) are essential in causing endodontic disease. |
|
Question 4: Define 4 key elements to managing endodontic infections.
|
The primary treatment of endodontic infections is to establish and maintain surgical drainage and to remove the cause of infection.
Maintaining drainage in combination with antibiotics is the correct treatment. Without adequate local drainage, fatal brain abscesses are possible. Persistent pain is indicative of a continued need for drainage. Apical healing can take months. |
|
Question 6: Name 6 species commonly isolated from root canal infections.
|
bacteroides
prevotella lactobacillus streptococci clostridium fusobacterium |
|
Question 7: State how you would collect a clinical sample from a peri-apical abscess and how you would use this sample to determine the ideal treatment option for a patient.
|
- Collection of pus by needle aspiration or after excision
- Aseptic technique - Swabs are highly prone to contamination by saliva and dental plaque flora Since most infections are due to strict anaerobes samples must be appropriately handled and dispatched Once the pathogen is identified, specific antibacterials can be prescribed??? |
|
Question 8: Give 4 possible clinical presentations of suppurative Osteomyelitis of the Jaws.
|
Inflammation of the bone leads to venous stasis, ischemia and pus formation.
May cause soft-tissue abscesses on the oral mucosa. Acute form-pain and fever Chronic form-tenderness |
|
Question 9: Describe the affect of calcium hydroxide (in seals in endodontics) on oral microbes.
|
high alkalinity to kill bacteria.
|