Perio Flashcards
What is periodontitis?
Periodontists is a multi factorial, inflammatory diseases associated with dysbiotic microbial dental biofilms and characterised by non-reversible progressive periodontal tissue destruction. It manifests through: CAL, radiographically assessed alveolar bone loss, presence of periodontal pocketing, gingival bleeding and leads eventually to tooth loss.
What are the main points of the old, Non-specific Plaque Hypothesis?
- All plaque bacteria are equally pathogenic
- Quantity of plaque determines the pathogenicity
- Host has threshold capacity to detoxify bacterial products
- Disease develops if threshold is surpassed
Treatment: non-specific mechanical removal of total amount of plaque
What are the main points of the Specific Plaque hypothesis?
- Due to advancement of microbiological technologies, specific bacteria that are believed to be pathological to the periodontium were isolated
- Not all plaque is equally pathogenic
- Presence and increase of specific microorganism causes more destruction
Treatment: targeting and elimination of specific microoganisms using antimicrobials
What are the main points of the ecological plaque hypothesis?
- Disease is the result of an imbalance in the total micro-flora due to ecological stress
- Quantitative plaque increase changes local micro-environment promoting the growth of specific pathogens, qualitative shift
- Ecological factors such as the presence of nutrients and essential cofactors, pH and redox potential
Treatment: prevention of dental caries, modification of micro-environment to prevent nourishment of pathogens
Explain, briefly, the Yellow, orange and red groups that were suggest by Dr. Socranky research of 1998. Please include the names of at least 3 different bacteria in all of the groups.
- The yellow, orange and red groups are suggested groups of bacteria that are associated with periodontal health and pathology
- Yellow group - include: S. Mitis, S. Oralis and S, Snagius - are early coloniser groups that are related to healthy periodontium
- Orange group - include: P.Intermedia, P.Nigrescens and F. Nucleatum - are late coloniser that are believed to be an intermediate step and are able to facilitate red group (the most pathogenic group) in binding in the periodontal pocket
- Red group - include: P. Gingivalis, T.Forsythia, T. Denticola - believed to be the most pathogenic group
What is the microbial virulence?
Virulence is defined as the degree of pathogenicity of the ability of the organism to cause disease measured in experimental procedures.
Organism need to:
- Attach and colonise
- Multiply and gain access to appropriate nutrition
- Evade host defences
- Propagate
What is A. Actinomycetemcomitans?
A. Actinomycetemcomitans or AA is a gram negative anaerobe that is associated with localised aggressive periodontitis.
Able to produce high level os leukotoxins thus causes the lysis of PMNs.
It is equiped with adhesis and invasisn which means it can penetrate the tissue and attach to the space it has penetrated
What is P.Gingivalis?
P. Gingivalis is a gram negative anaerob that is associated with periodontits (around 79-90% of perio cases will have this bacteria)
Main cause of the inflammation to the tissue - release of endotoxin (name: P.Gingivalis LPS)
Contains invasins, adhesins and also collagenases which degrade connective tissue.
What are the main points of the Keystone Pathogen Hypothesis & Polymicrobial synergy and Dysbiosis Model?
- Keystone pathogens (e.g. P.Gingivalis) trigger inflammation even in low numbers
- Causes normal microbiome to become dysbiotic
- Manipulation of native immune responses of host
- Inflammatory byproducts sustain dysbiotic microbiota
Treatment: host modulation in adjunct to direct antimicrobial measures
What are inflammophilic bacteria?
Bacteria that are able to propagate using by-products of inflammation
What are the stages of the IMPEDE model
Stage 0 - gingival and periodontal health
Stage 1 - gingival inflammation
Stage 2 - Polymicobial emergence
Stage 3 - Inflammation - mediated dysbiosis - initial perio
Stage 4 - Late stage periodontitis
What is the consensus on how periodontal destruction actually occur?
It is widely believed that periodontal destruction occurs due to effects of the immune response and not directly due to bacteria. 80 immune response, 20 bacteria.
What is the aetiology of periodontitis?
- Predominance of PMNs in pocket epithelium/activation in connective tissue
- Elevated activity of macrophages
- Plasma cells dominate the infiltrate
- Increase of pro-inflammatory cytokine production (like IL-6 and IL-8 and more)
- This results in disturbed tissue homeostasis leading to destruction of collagen, connective tissue matrix and bone
- This results in true pocket development from the junction epithelium
What are MMPs?
Matrix metalloproteinases (MMPs) are a large family of calcium-dependent zinc-containing endopeptidases, which are responsible for the tissue remodeling and degradation of the extracellular matrix (ECM), including collagens, elastins, gelatin, matrix glycoproteins, and proteoglycan.
They are regulated IL-6 and IL- 8.
They are released by many cells like PMNs.
What causes bone resorption?
- RANKL - produced by osteocytes in large quantities, due to stimulation of pro-inflammatory cytokines like IL-6 and IL-8, able to activate osteo clasts - bone resorbing cells
- RANK - receptor on osteocalst - binding site of RANKL
- OPG - scavenger receptor that prevents RANKL binding thus preventing bone resorption
RANKL:OPG ratio: relative amount regulate the bone turn over
What is the importance of T helper cells in periodontitis?
They help to propagate the process of secretion of pro-inflammatory cytokines and messengers
What is a risk factor?
Health risk factor are attributes, characteristics or exposures that increase the likelihood of a person developing a disease or health disorder.
What are some of the pre-disposing factors for periodontitis?
Any factor that result in retention of biofilm or prevents ts removal thus predisposing for disease progression.
E.g.:
Anatomical factors: root proximity, tooth malposition, concavities and furcation
Aquired/Iatrogenic factors: overhangs, open contacts and appliances
All this needs to happen in a susceptible host.
What are modifying or systemic factors?
They are factors that modify disease expression and may influence disease progression by altering host’s immune response
e.g. in periodontitis: smoking and diabetes
How does smoking increases the risk of periodontitis and by how much on average does it increase the instance of periodontitis according to latest studies?
The mechanisms:
1. Chronic reduction in blood flow and vascularity
2. Increase the prevelance of potential periodontal pathogens in the sulcus
3. Shift in neutrophil function towards destructive activities
4. Shift to a dysbiotic, pathogen enriched microbiome
5. Affects PMNs making them more aggrevated
6. Increase the number of aggravated T cells that produce inflammatory cytokines
It increases the risk of periodontitis by 85%!
Smoking cessation has beneficial effect on therapy outcomes and disease progression - this should be attempted for patient with nicotine dependence/
What are two useful statistics to give to a smoker patient in order to discourage them from smoking?
- Regular smokers have around 50% less improvement in clinical parameter after nonsurgical therapy
- Regular smoker have 2x implant failure rate compared to nonsmokers
How does diabetes increases the risk of periodontitis and by how much on average does it increase the instance of periodontitis according to latest studies?
- No solid evidence of causal relationship between poorly controlled diabetes and periodontal microbial dysbiosis in humans, but there some evidence in vitro thus it is biologically plausible
- Osteogenesis reduction due to apoptosis of osteoblasts and PDL fibroblasts
- Increase in RANKL expression and OPG expression is decreases
- Increase in collagenase activity
It increases the risk of periodontitis by 3x to 4x!
Multidisciplinary control and treatment of diabetes is ESSENTIAL to treatment of periodontitis.
What can be seen intraorally in a patient with diabetes and perio?
- No specific phenotypic features
- Pronounced clinical and radiographic signs
- Signs of progression
- Multiple reoccuring periodontal abscesses
- Unpredictable responses to therapy
- Increases risk of future attachment loss
If you suspect undiagnosed or poorly controlled diabetes, refer to GP for further investigations or management
What is the relationship between diabetes and periodontitis?
There is a bi-directional relationship between diabetes and periodontitis, meaning improvement in diabetes improve periodontitis but also improvement in periodontitis improve diabetes!
What are the common genetic defect that may cause periodontitis?
- Neutrophil disorders
- Single nucleoitd polymorphisms
Periodotitis is associated with variations in up to 20 genes.
Most forms of periodontitis are polygenic, being caused by a combination of genetic and environmental factors.
How do you write a diagnostic statement for diabetes?
- Type of periodontal disease
- Disease extent
- Stage
- Grade
- Current disease status
- Risk factor profile
E.g.
Periodontitis: generalized (65%), Stage III (CAL <10 mm), Grade C (HbA1c 8.9%), currently unstable (PPD <8mm, BOP 45%).
Risk factors: uncontrolled diabetes (HbA1c 8.9%), smoking 20 cig/day, high strss levels (change in work)
How do we calculate clinical attachment loss?
Pocket depth + recession or pocket depth - over growth or pocket depth
Is periodontal disease rare ?
No - very very common - both gingivitis and perio are pretty common
What is prevalence?
It refers to the total number of individuals in a population who have a disease or health condition at a specific period of time, usually expressed as a percentage of the population.
What is incidence?
It refers to the number of individuals who develop a specific disease or experience a specific health-related event during particular time period.
What have the 70-80s research into Sri Lankan tea labourers showed us?
- 10-15% resist periodontitis
- 10-15% have rapid progression
- 70-80% have moderate progression
How can you link back the instances of severe periodontitis with the current classification standards?
It was discovered, that on avergaere, people with sever cases of periodontists have attachment loss of around 0.45mm per annum.
Thus in the new classification, Grade C (fast progressing) is considered to be when an individual has a rate of progression of more than 2mm per 5 years (5 x 0.45)
What is one of the findings from studies relating to periodontal health in Australia?
Rates of periodontitis have remained relatively the same yet the tooth retention rate has been improving
What levels are we aiming at when we are discussing a plaque index?
We are aming at below 20% as it is essential for stable periodontal and peri-implant health over the long-term.
What BOP score are we aiming to achieve?
BOP score of less or equal to 20% because that is associated with significantly lower risk of CAL progression and want the score to decrease continuously and keep stable.
What the Community Periodontal Index of Treatment Needs codes and what treatment do they need?
Code 0 - healthy - treatment: home care
Code 1 - bleeding on probing but no attachment loss - treatment: oral hygiene instructions
Code 2 - calculus present + BOP - treatment: calculus removal and scaling + OHI
Code 3 - pockets of below 5 mm - treatment: calculus removal and scaling + OHI
Code 4 - pockets of above 6 mm - treatment: complex therapy + calculus removal and scaling + OHI
What is the first group of systemic diseases and conditions that relate to periodontitis?
They are some rare/uncommon systemic diease and conditions that cause a profound loss of periodontal tissues and usually early onset (may be in deciduous teeth).
Periodontitis might be one of the signs of these diseases.
Some of these disorders are:
1. Genetic disorders:
1.1. Down syndrome - aetiology not known but there is a link with damped immune function - occurs in adolescence in term of perio
1.2. Leukocyte adhesion deficiency syndrome - PMNs can no longer integrate - related to the integrin beta2 receptor thus GP will test for that - usually can be observed in child hood in terms of periodontitis
1.3 Papillion LeFevre Syndrome - reduces PMN function (NETosis) - results in early onset periodontitis in 1-5 year olds
1.4 Cyclic neutropenia - reduction in number of PMNs every 21 days for 3-4 days - reduction of periodontal tissue expected
1.5 Primary immunodeficiency diseases - not known
1.6 Plasminogen deficiency - enlarged and ulcerated gingiva with white membrane
1.7 Multiple metabolic & endocrine disorders
- Aquired Immunodeficiency diseases:
2.1 Aquired neutropenia
2.2 HIV infection - increased risk of opportunistic infections like necrotising periodontal diseases and other - Inflammatory disease:
3.1 Inflammatory Bowl Disease
3.2 Arthritis
What is the second group of systemic disease and conditions that relate periodontitis?
They are some relatively common systemic conditions that have a moderate impact on prevalence / severity of priodontitis.
These diseases usually have an influence on the parthenogenesis of periodontal disease.
Some of these disease and disorders are:
1. Diabetes
2. Obesity
3. Osteoporosis
4. Arthritis - could through are process of inflammatory aggravation called citrulination
5. Stress and depression
6. Hypertension - maybe but probably not - but people with perio are more likely to have hypertension
What is the third group of systemic disease and conditions that relate to peridontitis?
They are systemic or local conditions that mimic periodontitis and cause destruction of periodontal attachment. They are independent of plaque induced periodontitis and cause periodontal tissue damage through other mechanisms.
Some of these disease and disorders are:
1. Neoplasm that originate from the gingival and may resemble perio
2. Giant cell granuloma and many other very rare diseases that may mimic symptoms and signs of perio
What are some of medications that have a negative impact on the periodontal tissue?
- Anticancer chemotherapy - leads to neutropenia
- VEGF inhibitors - delay wound healing but still needed for chemo
What are some of the medications that have a positive impact on the periodontal tissue?
- NSAIDs - general anti-inflammatory effect
- Anti-TNF therapies
What is the theory of “direct pathway” that connects periodontal health with systemic health?
It believed that due to increased number of bacteria and smaller barrier to penetrate (ulcerated epithelial pocket lining).
1. The ulcerated periodontal pocket liing acts as a gate for viable bacteria, bacterial toxins/componetns
2. It results in frequent transient bacteremia
3. And could result in substantial systemic inflammatory response
This pathway also goes via other organs and systems like during swallowing or inhalation.
Important to understand that systemic bacteraemia as a result of periodontal infection is rare.
There is actually a way you can calculate periodontal inflamed surface area thus it is important to reduce that area with treatment.
What is the theory of indirect pathway?
It also relates to the periodontal inflamed surface area.
It is a theory that states that affects on the systemic health from periodontal disease result due to pro-inflammatory mediators that are involved in periodontitis.
Less plausible than the direct pathway.
What is the association between periodontitis and atherosclerotic coronary vascular disease?
AVD is the most common form of death worldwide.
It is a result of vascular inflammation and subintimal lipid accumulation which could result in build up of atheroma, stenosis of the valves, rupture of blood vessels and thrombosis.
There is some evidence to suggest there is association between the A.a. bacteria and P. Gingivalis being recovered from human atheromas. Thus an increase in those bacteria may result in increases risk of atheromas. These bacteria may effect the endothelia walls, immune function, impact macrophage function through different mechanisms.
