Intro to gingival and periodontal diseases Flashcards
Periodontology definition
the study of the periodontal tissues in health and disease; including the causes, prevention and treatment of diseases of the periodontal tissue
What makes up the periodontium (periodontal tissues)?
gingivae, periodontal ligament, root cementum, alveolar bone
What is the border between the enamel and cementum known as?
Amelocemental junction (ACJ) / cementoenamel junction (CEJ)
What are the two types of gingiva?
free gingiva and attached gingiva
What forms the seal between the enamel and gingiva at the bottom of the sulcus?
Junctional epithelium
What is the difference between a sulcus and pocket?
A sulcus is the healthy 1-3mm gap between the free gingiva and the tooth. An inflamed sulcus is known as a pocket.
Size of healthy sulcus
1-3mm
What determines an individuals periodontal health?
The balance between bacteria of the dental plaque and the host immune system
Periodontal disease definition
a group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque.
How can periodontitis be prevented?
By catching it at the gingivitis stage and doing screening BPE twice a year
Difference between gingivitis and periodontitis
gingivitis is reversible whereas periodontitis is life-long. Gingivitis only involves soft tissues whereas periodontitis involves bone loss too (which can lead to tooth loss)
What percentage of the entire world population is estimated to have periodontal disease?
~70%
Why is periodontitis a significant disease?
Periodontitis is a risk factor for systemic disease e.g. rheumatoid arthritis, CVD
Inflammation definition
Biological response to remove harmful stimuli (e.g. pathogens, damaged cells, irritants) and to initiate healing.
Cardinal signs of inflammation
Pain, heat, swelling, redness, loss of function (e.g. bone loss)
Why is it a problem that periodontitis does not cause patients much pain? (as it’s a small tissue)
Patients can ignore blood (but not pain like in pulpitis). Dentists can’t detect periodontitis early to put it into a stable stage. Patients may only come to dentist when teeth become mobile which is too late (only 10-20% bone left)
Effects of inflammation
vasodilation, increased permeability of vessel walls, inflammatory exudate, emigration of WBCs from blood vessels into connective tissue (diapedesis)
Why is periodontitis chronic inflammation?
There is no resolution of inflammation
Etiopathogenesis definition
cause and development of a disease
Factors that can contribute to the development of periodontal disease
general health, immune system function, genetics, other pathological conditions
Aspects of general health that can contribute to periodontal disease
stress, fatigue, smoking, diet, hygiene habits, medications
Examples of pathological conditions that can contribute to the development of periodontal disease
viral infections, bacterial infections, diabetes mellitus, hypoxia, liver disease
Example of acquired local risk factors for periodontal disease
plaque, calculus, overhanging, poorly contoured restorations
Examples of anatomical local risk factors for periodontitis
malpositioned teeth, root grooves, concavities and furcations, enamel pearls (ortho-perio synergy)
How can local risk factors contribute to periodontal disease development?
intensify plaque accumulation
non-modifiable systemic risk factors for periodontal disease
ageing, genetic factors
modifiable systemic risk factors for periodontal disease
smoking, poorly controlled diabetes, stress, medications, hormonal changes, poor nutrition, socioeconomic status
What was the non-specific plaque theory of the 19th century?
accumulation of dental plaque was responsible for oral disease without discriminating between bacterial virulence
What was the specific plaque theory of the 20th century?
few species of the total microflora are actively involved in disease
What was the ecological plaque theory of the 20th century?
changes in the environment (e.g. pH, redox) can favour the growth of certain bacterial species (composition of plaque depends on environment)
What has been the most recent theory about periodontal disease?
Polymicrobial dysbiosis theory and Keystone-pathogen hypothesis
What is the polymicrobial dysbiosis theory and the keystone-pathogen hypothesis of the 21st century?
certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodelling the microbiota into a dysbiotic one.
Example of a keystone-pathogen
Porphyromonas gingivalis
Biofilm definition
an aggregate of microorganisms that adhere to each other on a (living/non-living) surface. The adherent cells are embedded within a self-produced matrix of EPS
What is EPS?
Extracellular Polymeric Substance - a matrix made of DNA, proteins, polysaccharide
Why is biofilm advantageous to bacteria?
Resistance to antibiotics, antibacterial agents and mouthwash (cannot penetrate), hidden from immune system of host
Where can biofilm form?
Living or non-living surfaces in natural, industrial and hospital settings. Can form in water and sewage pipes.
Difference between biofilm and planktonic bacterial growth?
Planktonic bacteria are free-living so are not protected by biofilm and can be treated with antibiotics.
What is dental plaque?
A type of biofilm found subgingival and supragingival tooth surface
Why can the concept of commensal and pathogenic bacteria be twisted?
Because some ‘commensal’ bacteria can assist pathogens - infections are polymicrobial not monomicrobial. Porphyromonas gingivalis is unable to trigger disease without presence of other bacterial species.
How can you visualise dental plaque?
using disclosing agent
What is the dental pellicle?
A protein film formed by proteins and glycoproteins in saliva a few minutes after brushing. Protects against acidity and is important in remineralisation.
How does biofilm form?
- dental pellicle forms in a few minutes
- Trailblazing bacteria (Streptococcus, Actinomyces) can adhere to pellicle
- growth of microcolonies and production of polysaccharide matrix (EPS)
- transition of mature biofilm colonies into metabolic complexes
How do bacteria cooperate?
Bacteria have different enzymes so can form a chain of metabolism so each species has access to nutrients. Range of virulence factors protects whole colony.
How have pathogens been categorised based on their association with the severity of periodontitis?
Socransky’s complex
What are keystone bacteria?
certain low-abundance microbial pathogens that can cause inflammatory disease by changing the composition of normal microbiota and interfering with the host immune system
In which of Socransky’s complexes is Porphyromonas gingivalis located?
red complex
Why does Porphyromonas gingivalis manipulate the host immune system?
P. gingivalis needs iron from hemin in GCF so bleeding due to inflammation will aid survival. However, P. gingivalis needs to avoid the immune system.
How does Porphyromonas gingivalis cause inflammation?
By manipulating toll-like receptor response. P.gingivalis has LPS type 1 which is a TLR4 agonist (activates immune response), and LPS type 2 which is a TLR4 antagonist (blocks receptor once there is enough bleeding/inflammation)
How does Porphyromonas gingivalis escape the host immune system?
- local chemokine paralysis (innate)
- corrupts complement system (adaptive)
- invade keratinocytes to hide
How does Porphyromonas gingivalis cause local chemokine paralysis?
P. gingivalis secretes serine phosphatase which inhibits the synthesis of IL-8 so there is a low chemokine concentration near the pathogen.
Why does periodontitis cause damage to the periodontium?
Immune cells (e.g. neutrophils) enter the invaded tissue via diapedesis. However, as P. gingivalis breaks down IL-8, immune cells do not phagocytose P. gingivalis and instead break down the surrounding periodontium.
How does Porphyromonas gingivalis corrupt the complement system?
Gingipains arginine-specific cysteine proteinases cleave complement factors C3 and C5. P. gingivalis therefore avoids complement-mediated detection and destruction.
How could someone’s immune system make them more susceptible to periodontitis?
An overly active immune system can launch inflammation against own biofilm (healthy, aerobic bacteria) leading to destruction of periodontium. Or an impaired immune system that has a lack of protection (leads to acute periodontitis)
Why may an individual’s immune system be impaired?
genetic condition or disease
Examples of genetic conditions associated with impaired immune system
Papillon-Lefevre syndrome, Chediak-Higashi syndrome, LAS syndrome, Down’s syndrome, chronic granulomatous disease
Examples of diseases leading to impaired immune system
Leukaemia, agranulocytosis, neutropenia, HIV
How is calculus formed?
By calcification of dental plaque
Why can a small amount of calculus lead to faster formation of more calculus?
Calculus is a plaque retention factor
Clinical signs of gingivitis
erythema (redness), swelling, bleeding on gentle probing, (no deep pockets unlike periodontitis)
Patient complaints from periodontitis
bleeding on brushing, halitosis, bad taste, sensitivity, drifting teeth, mobility, discomfort
Why can periodontitis cause teeth sensitivity?
Bone recession can expose root surface. Cementum is worn down quickly so dentine is exposed which contains nerve endings
When can periodontitis be painful?
rarely - mostly in necrotising periodontal disease
Clinical signs of periodontitis
bleeding on gentle probing, erythema, loss of knife edge margin, halitosis, swelling (false pocket), bone loss, true pocket, recession, mobility, purulence
Difference between a false and true pocket
false pocket is due to gingival swelling whereas a true pocket is due to loss of attachment (exposed root surface)
Furcation definition
bone loss in between roots
What will you need to warn the patient might happen when inflammation decreases?
During inflammation, gingival swelling will cover root surface despite bone loss. However, when inflammation decreases, swelling will decrease so gingival recession will be more prominent, root exposed, sensitivity. Sign of success (can block dentinal tubules)
