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PERIO - NEW SET FOR FINALS > PERIO > Flashcards

PERIO Flashcards

1
Q

What can perio be classed into?

A

Health and Disease

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2
Q

HISTOLOGICALLY, what does gingival HEALTH look like?

A

There is still evidence of the presence of inflammatory cells (neutrophils) in the gingival connective tissue, even after seconds of brushing, plaque starts to accumulate causing VASODILATION - there may not be a clinical sign of inflammation, but histologically there is.

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3
Q

What are the CLINICAL signs of clinical gingival health

A

Pink/Pale gingiva
Stippling (orange peel effect) - this is caused by the arrangement of the connective tissue underlying gingivae - tight epithelium (lots of collagen)
Knife edge margins
No BOP/inflammation present

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4
Q

What are the CLINICAL signs of a gingivitis (5)

A

Red
Swollen
Rolled margins
BOP
Loss of stippling

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5
Q

Describe the aetiology of gingivitis (how is it caused)

A

all to do with the QUANTITY of plaque
the plaque will initiate an inflammatory response
over more than 7 days, we will have mature plaque meaning greater thickness, gram -ve anaerobic bacteria (facultative) start to appear - microbial succession causing GINGIVITIS

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6
Q

Describe the stages we can get from gingivitis (3)

A

can either:
- stay the same
- regress
- progress onto periodontitis

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7
Q

What are the clinical signs and symptoms of PERIODONTITIS (9)

A
  • increased probing depth
  • bleeding
  • mobility
  • furcations
  • shrinkage
  • halitosis
  • plaque
  • calculus
  • pre-existing gingivitis
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8
Q

Describe the AETIOLOGY of periodontitis (how is it caused?)

A

bacteria (PLAQUE), Poor OH
RISK factors Local and Systemic

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9
Q

Describe some SYSTEMIC risk factors that can increase the risk of periodontal disease

A

immunocompromised (medical conditions) , diabetes, smoking, genetics, age

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10
Q

Describe some LOCAL risk factors that can increase the risk of periodontal disease(5)

A

Overhangs, restoration deficiencies, calculus, tooth anomalies, appliances - orthodontic or dentures that are ill fitting.

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11
Q

Describe how smoking can effect the periodontium HISTOLOGICALLY (on a cellular level)

A

Smoking causes VASOCONSTRICTION in the gingival tissues, this in turn restricts the number of host cells entering the gingival tissues through the blood, therefore, there are less neutrophils (PMNL’S) and macrophages (monocytes when OUTWITH tissue in bloodstream). Due to the lack of neutrophils rushing into the site due to the vasoconstriction, we get less fibroblast production and therefore no laying down of collagen

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12
Q

Describe what we can see CLINICALLY in a smokers periodontium (9)

A

smokers have:
- more calculus
- plaque
- spend less time brushing teeth
- more alveolar bone loss
- deeper pockets
- more vertical defects
- hyperkeratinised tissue
- REFRACTORY response is impaired to NSPT
- Healing is impaired

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13
Q

Describe how Diabetes can affect the periodontium

A

an increase in glucose molecules within the blood can impair the host response and increase the levels of disease/healing process post NSPT - THIS IS ONLY IN POORLY CONTROLLED DIABETES!
Diabetes increases the risk and severity of periodontal disease. Factors that contribute to this include slowed circulation, which can render gum tissue susceptible to infection, and lowered body resistance to infection, which increases the probability of gums becoming infected. Individuals with Type II diabetes face a higher risk of developing gum disease because their immune response does not develop antibodies to pathogens associated with periodontitis.

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14
Q

List the different types of Acute Periodontal Conditions (5)

A

Necrotizing Gingivitis
Necrotizing Periodontitis
Pericoronitis
Periodontal Abscess
Acute Herpetic Gingivostomatitis

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15
Q

Describe the AETIOLOGY of Necrotizing Gingivitis (how is it caused)

A

This is a fuso-spirochetal infection, caused mainly by TREPONEMA VINCETIL along with Fuso Nucleatum, Prevotella Inter, treponema denticola - all GNABs

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16
Q

Describe the RISK FACTORS that may make us succeptible to NG (4)

A
  • immunocompriomised
  • Poor OH
  • Smoking
  • Stress
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17
Q

Describe the clinical signs/symptoms of NG (12)

A
  • grey pseudomembranous slough
  • foetor oris
  • Red, angry, severely inflamed gingivae
  • SPONTAENEOUS bleeding
  • ‘punched out’ papillae
    -ulceration
  • pain
  • general malaise
  • fever (sometimes)
  • lymphadenopathy
    -metallic taste
  • in extreme cases, if left untreated, we can get facial necrosis
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18
Q

What is the MANAGEMENT OF NG(4)

A
  1. OHI/smoking cessation
  2. Prescription of metronidazole for 3-5 days (400/500mg 3 times a day)
  3. USS (1st reason for the CAVITATIONAL effect to kill anaerobic bacteria, 2nd reason for a cooling effect on gingivae - pts like this sensation)M
  4. Review condition in 7 DAYS - further PMPR/advice
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19
Q

Describe the AETIOLOGY OF Necrotizing Perio

A
  • ALWAYS preceded by NG
  • all else is the same
  • Histopathology is slightly different in that it is bone loss and PDL loss
  • clinically, we can often see exposed bone (v nasty disease)
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20
Q

Describe what pericoronitis is

A

Usually occurs on PE teeth, operculum causes plaque to get trapped under resulting in inflammation and infection

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21
Q

What is the AETIOLOGY of a perio abscess

A

Bacteria not being able to exit the blocked pocket, this blocked pocket may be from calculus, food, a scaling in which there has been a bit of dislodged calc that has gotten stuck.
EXISTING PERIODONTITIS IS A RISK FACTOR OF TIS TYPE OF ABSCESS

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22
Q

What is the MANAGEMENT of a perio abscess

A
  • sometimes a course of antibiotics
  • scaling/PMPR carried out to flush away debris
  • Review
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23
Q

What are the clinical signs and symptoms of a perio abscess

A
  • swelling of face
  • pain
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24
Q

Describe the Aetiology of Acute Herpetic Gingivostomatitis

A

Caused by herpes simplex 1 virus (hsv-1)

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25
Q

What are the clinical signs and symptoms of AHG (8)

A
  • generalised erythema (redness)
  • pain
  • all over mouth
  • around vermillion border
  • ulceration (yellow hue)
  • lymphadenopathy
  • fever
  • general malaise
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26
Q

What is the management of AHG

A

Due to it being a viral infection, ABs are not involved - therefore, we would treat this with analgesia and control temperature

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27
Q

Describe the complication of of AHG

A

due to it being a virus, it lies DORMANT to the trigeminal ganglion

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28
Q

How can AHG be reactivated ?

A

can be reactivated by:
- immunosuppresion
- stress
- exposure to UV light (sunlight)

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29
Q

What is the clinical sign of reactivated AHG

A

Herpes Labialis (coldosre)

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30
Q

What are the two main areas of management within perio

A

PREVENTION (plaque control)
NSPT (instrumentation)

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31
Q

Describe 3 main mechanical plaque control methods for prevention in perio

A

OHI - TBing techniques (what types), ID cleaning (what types)- MECHANICAL PLAQUE CONTROL ALWAYS TAILORED TO INDIVIDUAL, PMPR (removal of calculus removing retentive for plaque to adhere to) (explain each of these further)

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32
Q

What is important to consider when providing OHI to a patient

A

Need to consider pt motivation, and effects of non-compliance. We should always concentrate on the positives! keeps pt morale high

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33
Q

Describe some methods of chemical plaque control for prevention of perio

A
  • toothpaste - fluoride and triclosan
  • mouthwashes - chlorohexadine, phenol, oxidising mouthwashes
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34
Q

Describe some adv and dis of using chlorohexadine mouthwash

A

Adv - is that is has bisbiguanide in it which is a plaque inhibitor
Dis - can cause gross staining, can alter the function of taste buds, associated with calculus formation, can effect the efficacy of salivary glands

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35
Q

Describe the adv and dis of using phenolic mouthwashes

A

adv - is that it has a slight antibacterial function - very short lasting
Dis - use after brushing which washes fluoride away, increase in alcohol content increasing the risk of OC (cosmetic mouthwash like Listerine)

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36
Q

Describe the adv and dis of oxidising mouthwashes

A

Adv is that it contains hydrogen peroxide which can act as a cavitational effect and kill bacteria which can be effective for conditions such as NG

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37
Q

why do we carry out NSPT (non-surgical perio treatment)

A

TO RENDER THE ROOT SURFACE BIOLOGICALLY COMPATIBLE WITH HEALING or DISRUPT THE BIOFILM

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38
Q

HOW do we carry out NSPT

A

By instrumenting the root surface by using :
USS, hand scalers

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39
Q

Describe the sequence of treatment carried out in NSPT and why are we doing it

A
  • pre USS in order to: disrupt the plaque biofilm and break up large calculus deposits
  • hand scale - for fine tuning
  • post USS - flush out any remaining debris
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40
Q

What is the sequence planning for RSD / why

A
  1. OHI
  2. 6 ppc (why? - because it gives us a more DETAILED view of disease present in mouth, and also provides pts with motivation as it is almost like a visual aid
  3. supra and sub PMPR (professional mechanical plaque removal) - NSPT
  4. review ppds in 3/12.
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41
Q

Describe 3 states a patient will either be post rsd treatment at the 3/12 review

A

STABLE, NON RESPONSIVE, PARTLY RESPONSIVE

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42
Q

What action do we take if a patient is in a stable state post rsd/treatment?

A

Maintenance Therapy (or also called supportive periodontal therapy - SPT) - THIS IS ONLY FOR PTS WHO HAVE A STABLE PERIODONTIUM and is tailored to the individual

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43
Q

Describe the PATHOGENESIS?HISTOPATHOLOGY of the progression to perio disease/how does plaque develop on a tooth (4)

A
  1. Within seconds of brushing - plaque bacteria sticks to tooth by the acquired pellicle (aerobic, gram positive eg streptococci) - NOT MUCH DAMAGE TO PERIODONTIUM HERE
  2. Within hours: Bacteria will multiply causing layers of plaque to develop however, it is still simple anaerobic bacteria here along with rods, lactobacilli and actinyomyces
  3. After 7 days (or more), we not have mature plaque on surface of tooth, therefore the thickness is increased. In the deeper layers we will now get gram -ve anaerobic (facultative) bacteria start to appear eg tanarella forsythia, treponema denticola. THIS RESULTS IN GINGIVITIS
  4. PERIODONTITIS develops
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44
Q

What 3 paths can gingivitis take?

A

can either stay the same, regress, or progress onto periodontitis

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45
Q

What are the 4 lesions called from the page and schroeder (1976) study?

A
  1. initial lesion
  2. early lesion - 1/2 both EARLY stages of gingivitis
  3. established lesion - clinically obvious gingivitis
  4. advanced lesion - periodontitis
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46
Q

Describe the INITIAL LESION (4)

A
  • 24-48 hours plaque accumulation
  • vasodilation of blood vessels, increase in neutrophils, increase in GCF - THIS IS ALL BELOW THE JE
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47
Q

Describe the EARLY LESION

A
  • After 1 week
  • fibroblasts are destructed, therefore a decrease in collagen - THIS IS VERY MINIMAL
  • cytokines rush into site and immunoglobulins are produced (pro-inflammatory) released.
  • more inflammatory infiltrate so neutrophils and lymphocytes
  • increase in GCF
  • inflammatory swelling of gingiva results in deeper gingival crevice
  • favour the growth of -ve bacteria
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48
Q

Describe the ESTABLISHED lesion

A
  • 2-3 weeks
  • gingivitis is CLINICALLY diagnosed/ESTABLISHED
  • gingival connective tissue largely replaced by inflammatory infiltrate
  • JE replaced by ulcerated leaky pocket epithelium - no longer attached to tooth
  • increased neutrophils in pocket
  • increase in immunglobulins
  • bacteria and host cells BATTLE causing damage
  • decrease in collagen
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49
Q

What do neutrophils do in host response

A

provide host defence mechanisms such as phagocytosis of pathogens

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50
Q

Describe/list some of the bacteria found in a perio pocket

A

Pg, Td, Tf (RED COMPLEX)
fn, Pi, Aa (ORANGE)

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51
Q

Describe what the bacteria do within the deep perio pocket (3)

A

They cause DESTRUCTION by:
-producing toxic material
- instigating the inflammatory/immune response
- they evade the host response

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52
Q

Describe some features of Porphyromonas Gingivalis

A

it has a capsule around it giving it a protective barrier called fimbrae

has gingipains -these are proteases which degrade cytokines thereby downregulating the host response
contains enzymes, toxins and acids

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53
Q

Describe the host response within periodontal disease

A

we can have either an inflammatory response or an immune response
inflammatory is fairly straight forward initiates the innate response
immune can be either innate (natural) or acquired

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54
Q

what does the inflammatory response involve within the host response

A

firstly VASODILATION (in response to plaque on tooth surface) of blood vessels occurs, meaning there is an influx of neutrophils (PMNL’S) and increased gingival crevicular fluid. The initial inflammation in the periodontal tissues should be considered a physiologic defence mechanism against the microbial challenge, rather than pathology (no immune cells involved here). The clinical findings of the disease at this stage include supragingival and subgingival plaque formation, which are usually accompanied by calculus formation and gingival inflammation. If plaque is removed, there is resolution with return to homeostasis; if the lesion persists, it becomes pathology. (PERIO - WHERE THE IMMUNE RESPONSE INS INVOLVED)

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55
Q

describe innate immunity within the host response

A

Innate immunity is the body’s first line of defence (is initiated by the inflammatory response - so is the specific/acquired) against pathogens and foreign invaders, including bacteria, viruses, and fungi. It provides immediate, NON-SPECIFIC protection against a wide range of potential threats.
Components of innate immunity include physical barriers (such as the skin), chemical barriers (such as saliva), and cellular components (such as neutrophils, macrophages, dendritic cells, and natural killer cells).

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56
Q

describe acquired immunity within the host response

A

this involves the release of ig’s, t cell lymphocytes and b cell lymphocytes (immune cells)

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57
Q

what role do t cells play in the acquired immunity response?

A

T-cells work once they’re activated.
- T-lymphocytes make up the cell mediated immune response. It is called this because the ANTIGEN SPECIFIC MOLECULE on the t-cell is not released from the cell, but remains stuck to the t-cell surface.
- SO, DIRECT, contact between the T-cell and bacteria is necessary to cause BACTERIAL DESTRUCTION!
- A cell called an antigen-presenting cell (APC) locates evidence of the intruder/foreign bacteria and attaches it to a structure called major histocompatibility complex (MHC).

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58
Q

what role do b cells play in the acquired immunity response?

A

When B cells encounter antigens (harmful substances like viruses or bacteria), they produce immunoglobulins which are antigen specific molecules. IgG, A, M, D, E. IgG is found in GCF, and IgA is found in the saliva - most important ones for perio disease.

59
Q

what role to Ig’s play in the acquired immunity response?

A
  • neutralise from bacteria
  • cause opsinisation - when they attach APC, antigen presenting cell made for destruction
  • there are 5 main classes IgG, IgA, IgM, IgD, IgE. THE MOST IMPORTANT IN PERIO DISEASE IS IgG and IgA - igG/A is within our saliva ! igG/A- GCF
60
Q

What are the 3 types of T cell Lymphocytes

A

Helper T cells - Assist in the maturation of B cells
T cytotoxic killer cells (kill foreign cells)
T memory cells - live in LYMPH NODES

61
Q

Following RSD, what are the CARDINAL symptoms within the first 24-48 hours?

A

ACUTE INFLAMMATION - swelling, redness, loss of function, pain, heat
CHRONIC - swelling/redness - over longer period of time

62
Q

what advice should we give our patients post RSD treatment

A

POIG term often used
May get some tenderness/swelling of gums over 24-28 hours/2 days or so - so to take analgesics as within recommended dose for pain relief
Some post-operative sensitivity as
over longer periods of time may get gingival SHRINKAGE exposing some root surface, therefore may get some sensitivity from this

63
Q

Post RSD treatment, what is the healing process

A

Over the 1-12 weeks of healing, we get acute inflammation so inflammatory cells so vasodilation eg neutrophils, gcf alll present at this site.
Over time, there is NEW attachment of the JE, now known as the LONG JUNCTIONAL EPITHELIUM. This is formed via hemi-desmosomes (epithelial cells)
- during this time, we get reduced inflammatory cell infiltrate meaning reduced redness
-reduced bleeding
-reduced swelling
- increase in fibroblast NUMBER AND ACTIVITY meaning increased COLLAGEN PRODUCTION which causes gingival shrinkage and tightening of the gingival cuff

64
Q

post RSD treatment, we get an increased number/activity of fibroblast production meaning more collagen turnover, what does this mean for the periodontium?

A

TIGHTENING OF THE GINGIVAL CUFF / shrinkage - elasticity remains in the tissues

65
Q

what does tightening of the gingival tissues mean for the periodontium

A

GINGIVAL SHRINKAGE! - from the new formation of the long je acts like a zip

66
Q

What cells are involved with innate immunity

A

neutrophils,macrophages (big eaters that ENGLUF bacteria!!! help to clear infection) and cytokines - NON SPECIFIC
neutrophils are motile and move towards the bacteria. we also get the release of cytokines which regulate and mediate the inflammatory response so they recruit inflammatory cells to the site.

67
Q

why do we wait 3/12 before touching a perio pocket post RSD

A

due to the GRANULATION tissue in pocket - a very delicate barrier (jelly-like) therefore WE DO NOT PROBE

68
Q

what are the potential reasons for failure post RSD treatment (7)

A

Poor OH
Smoker
immunocompromised
uncontrolled/undiagnosed disease
gingival overgrowth
operator (esp furcation areas) have left calc remaining as a plaque trap
genetically just have high susceptibility

69
Q

What are the options for non-responding areas post RSD treatment?

A

1st line of treatment is re-do RSD , review again in 3/12
if not working and oh is pristine:
REF TO A PERIO SPECIALIST
PERIO SURGERY
CHEMICAL ADJUNCTS

70
Q

List the different types of perio surgery - describe each (5)

A

Gingivectomy -excision of the gingivae by removing the pocket wall to gain better access etc. Can also be for removal of gingival overgrowth
Gingival graft
furcationplasty - reshaping of furcation to make it easier to clean
tunnel prep
flap surgery - a section og gingiva, mucosa, or both that is surgically seperated from underlying tissues to provide better visibility.
guided tissue regenration - a ‘neutral’ membrane is put directly onto root surface from cut back gingiva, either goretex/tephlon for around 6 months. this barrier is there to hold back the epithelial cells from dividing too fast and to allow the longer taking division of the ligament cells to grow back. These cells take around 6 months to lay down (new bone cells/ligament cells divide MUCH slower than epithelial cells!)
gingival attachment to root = new JE attachment

71
Q

What is the gold standard radiograph for perio disease

A

PERIAPICALS

72
Q

Describe the 4 different toothbrushing techniques

A
  1. Modified BASS technique - bristles are at a 45 degree angle pointing towards the gumline
  2. mini scrubb - horizontal / vigorous movements brushing technique
  3. modified stillman technique - aims to clean to underside surface of the teeth. As well as the gumline
  4. roll technique - brush is rolled over the gum line
  5. charters technique - for ortho appliances , 45 degree downwards and upwards for the bracket
73
Q

What is in calculus ?

A

Calcified DENTAL PLAQUE - CACLIUM and PHOSPHATE ions which is hardened by minerals in our saliva/found in our saliva too
endotoxins can escape through the pores from dead bacteria !!!!

74
Q

Describe the different codes and treatment guidance (to create a treatment plan) we use when doing a BPE

A

Code 0 - NO TX REQUIRED, pockets are less than 3.5mm
Code 1 - OHI - pockets are less than 3.5mm
Code 2 - OHI plus calculus removal and/or correction of plaque retentive restorative margins - pockets are less than 3.5mm

PATIENTS WITH BPE SCORES OF 0, 1, 2 IN ALL SEXTANTS SHOULD BE SCREENED AGAIN AFTER ONE YEAR. - low risk pts

Code 3 - OHI, scaling as INITIAL THERAPY, then if still code 3 - pocket charts should be recorded on areas of code 3’s & RSD as required (if initial therapy does not resolve things as we could have got false pocketing from initial exam! could be from gingivitis) - code 3 = 3.5-5.5mm
Code 4 or Code * - OHI, detailed pocket charts, plaque and bleeding too, then supra-sub ging pmpr, then review in 3/12 - probing depth = 5.5mm

75
Q

List some advantages of carrying out a BPE(7)

A

Seven main ones:
- it is a simple/rapid screening system which aids in the identification of those individuals with significant perio disease who then require a much more DETAILED perio examination
- the system is well recognised internationally, aiding in communication of info across geographical boundaries
- the examination is both rapid and easy to complete
- the only equipment needed is an appropriate probe - readily available and cheap
- system SUMMARISES the perio condition in a readily communicatible form
- the system as a whole gives an indication of treatment appropriate to the codes assigned and suggests in some codes whether referral should be considered.
- it encourages examination of the periodontal tissues in general practice as undiagnosed perio disease is one of the major causes of litigation in dentistry.

76
Q

List some disadvantages of carrying out a BPE(6)

A
  • Lack of DETAIL within sextants - no detail of the actual number of affected site or severity of involvement eg a 6mm pocket would be assigned a code 4 but so would a 12mm pocket …
  • lack of info on DISEASE ACTIVITY
  • inability to provide information on LOA
  • inability to differentiate between true and false pockets - false pocket is automatically given a 3
  • BPE cannot be used for young individuals LESS THAN 7
77
Q

Describe the grading system we use for mobility

A

MILLERS MOBILITY INDEX
Grade 0 - 0.2mm - this is normal physiological movement
Grade 1 - More than 0.2mm but less than 1mm
Grade 2 - more than 1mm - horizontal direction only
Grade 3 - more than 1mm - horizontal and any vertical movement means it is automatically a grade 3 mobile - whatever is going on horizontally does not matter

78
Q

Describe the grading system we use for measuring furcation’s

A

HAMP ET AL
Grade 1 - less than a 3rd of the way through
Grade 2 - more than a 3rd of the way through
Grade 3 - ALL the way through - through and through

79
Q

What can the main problem of patients having furcation’s be?

A

Furcation teeth can be more prone to infection flowing in and out - could further progress onto a perio abscess

80
Q

What is the onset of Necrotizing perio?

A

the onset can be from full blown AIDS

81
Q

What 2 things do we consider regarding SUCCEPTIBILITY to periodontal disease?

A

OH and age - it is not just the plaque levels to take into account - we need age along side this !

82
Q

What are the two TYPES of USS

A

MAGNETO-STRICTIVE - nickel/metal stacks allowing conduction right up to the vibrating tip
PIEZO-ELECTRIC - crystals in ceramic discs

83
Q

Describe the ADVANCED lesion (5)

A
  • transisiton from gingivitis - perio
  • ulceration and migration of the JE apically
  • gingival pockets are well established, attracting biofilm
  • breakdown of PDL fibres
  • alveolar bone undergoing RESORPTION (production of osteoclasts from activated cytokines releasing host resorption factors)
84
Q

What can we see clinically in diabetics with perio

A

Clinical symptoms of periodontal disease in diabetics include mouth ulcers, gingival inflammation, gingival recession, bleeding on probing, and persistent bad breath.

85
Q

What are the 5 CARDINAL signs of inflammation

A

Redness
Swelling
Heat
Pain
Loss of function

86
Q

What are the two types of pockets in perio

A

FALSE POCKET - base of the pocket is at or above the CEJ but NO LOA

TRUE POCKET - base of the pocket is below/apical to the CEJ there is LOA

87
Q

what is supra-gingival calculus (6)

A

= tends to be LIGHT yellow but can stain darker with food/drink and in smokers
= heaviest opposite openings of saliva ducts
- lingual lower incisors (submandibular duct)
- buccal upper molars (parotid duct)
=fairly hard and brittle
= easy to detect using probes and drying with 3 in 1 air

88
Q

What is sub-gingival calculus (7)

A

= forms within periodontal pockets, and is attached to root surfaces, which makes finding it difficult - detection requires gentle use of perio probes to feel for the subgingival calc on the root surfaces in the pockets
- sometimes seen on rads
- gingival recession may expose/uncover subging calc
= forms throughout the mouth, particularly where OH is inadequate
=dark green/black in colour
= v hard/tenatious and can be difficult to remove with instruments
- USUALLY REQUIRES RSD

89
Q

what is the primary cause of gingival/periodontal inflammation?

A

a BIOFILM is the name given to microbial communities attached to a surface.
PLAQUE = general term given for the microbial community found on the tooth surface - THIS CAUSES INFLAMMATION AT A SPECIFIC SITE

90
Q

what structure is found at the BASE of the gingival SULCUS extending to the CEJ

A

JUNCTIONAL EPITHELIUM (v important structure in perio health/disease) - the JE has wide spaces between the epithelial cells allowing plaque bacteria and their toxins to leak into the underlying gingival tissue causing inflammation
in DISEASE we can see apical migration of the JE

91
Q

in health. where does the JE extend to?

A

extends from the BASE of the gingival sulcus/sulcular epithelium to the cemento-enamel junction (cej)

92
Q

what is LOA (loss of attachment)

A
  • in health the base of the gingival crevice is at the CEJ
  • the CEJ is used as a fixed reference point in perio because it can be detected clinically or in rads
  • LOA is when the base of the pocket/gingival margin is below the CEJ ie on the root surface.
93
Q

What is gingivitis

A
  • REVERSIBLE biofilm/plaque induced inflammation of the gingival tissues with NO LOA NO bone loss
  • JE is replaced with pocket epithelium which is ulcerated (leaky) - pocket epithelium is not attached to the tooth , allowing apical migration of POCKET and the plaque biofilm. - false pocketing here
94
Q

what is periodontitis

A
  • biofilm/plaque induced chronic inflammation resulting in permanent loss of the periodontal support structures - LOA and true bone loss
  • ulceration and APICAL MIRGATION OF THE JE onto the root surface with breakdown of the pdl fibres further causing LOA - periodontitis is irreversible!!! - we can stabilise this disease
95
Q

What are the MODIFIABLE risk factors of periodontal disease (6 points)

A

A modifiable risk factor is one that can be CHANGED AS PART OF PATIENT MANAGEMENT :
oral hygiene = OHI
smoking = smoking cessation advice
diabetes - management by the pt/gp
alcohol = alcohol brief interventions
stress = counselling/mindfullness

96
Q

What is a risk factor relating to perio disease

A

RISK FACTOR = increases probability that a disease may develop in an individual: RISK FACTORS DONT CAUSE DISEASE, BUT WHEN PRESENT CAN MAKE IT WORSE (disease modifiers)

97
Q

What % of damage in periodontitis is due to the host response f the invading bacteria?

A

80%!!!!

98
Q

How can periodontal disease affect systemic disease ? (4)

A
  • the perio pocket is filled with a pathogenic anaerobic biofilm resulting in an inflammatory reaction etc resulting in the pocket wall being leaky.
  • because of this leaky wall, this allows inflammatory mediators to spill over into the systemic bloodstream leading to systemic inflammation potentially making other chronic diseases WORSE:
  • diabetes
  • cardiovascular disease (a couple - not exhaustive)
99
Q

what does LPS DO IN GRAM-NEGATIVE BACTERIA (ALSO IN GRAM POS )

A

LPS, otherwise known as endotoxin - can be found in calculus!!!!
Locally, it can stimulate inflammation and bone resorption, LPS in the blood can cause septic shock, hypotension/death.

100
Q

how do bacteria stick to the tooth?

A

the first step in dental plaque biofilm formation is attachment of the acquired pellicle to the tooth surface - the pellicle contains salivary lipids, proteins, and glycoproteins - THIS BINDING IS IRREVERSIBLE MEANING THE CAN RESIST SHEAR FORCES ie saliva flow and tongue movements.

We can get at the start, gram positive strep, then microbial succession of more harmful gram neg bacteria eg treponema denticola, p gingivalis - causing perio!!!

101
Q

What sort of drugs cause gingival enlargement?

A

Antiepileptic drugs - phenytonin, sodium valporate
Calcium channel blockers - amlodipine, verapamil
Immune regulators - cyclosporine (onset within 3 months of starting medication)

102
Q

List some of the CAUSES of non-dental biofilm induced gingival diseases (there are 8!)

A
  • genetic/developmental
  • specific infections (bacterial, fungal and viral)
  • inflammatory and immune conditions
  • reactive processes
  • neoplasms?
  • endocrine, nutritional and metabolic
  • traumatic lesions
  • gingival pigmentation
103
Q

Where may an endo-perio lesion occur?

A

May occur where an apical abscess has spread laterally

104
Q

What peri-implant diseases and conditions do we have?

A

PERI-IMPLANT HEALTH - absence of erythema, BOP, swelling and/or suppuration

PERI-IMPLANT MUCOSITIS - - bleeding on gentle probing, erythema, swelling and/or suppuration

PERI-IMPLANTITIS - inflammation, BOP and/or suppuration, increased ppds, radiographic bone loss compared to prev exams

PERI-IIMPLANT AND HT DEFECTS - includes any reduction of alveolar bone, due to tooth loss, trauma, systemic disease, medication etc

105
Q

Why is it important we eliminate calculus from a perio pocket? (4)

A
  • all calculus has a coating layer of dental plaque
  • supra calc impedes tooth brushing and ID cleaning
    • sub calc may absorb bacterial endotoxins
  • may impede perio probing, giving us a false probing depth
106
Q

What does full mouth disinfection involve (nspt)

A
  • this is a strategy for treating perio disease
  • aim - is to prevent REINFECTION of pockets by elimination of organisms as quickly as possible
  • conventional instrumentation and RSD within a 24 hour period along with OHI
  • also used along with a chemical adjunct such as chlorahexadine or an antibiotic duloxetine etc
107
Q

describe the 5 typical stages of a perio treatment plan

A
  1. INITAL ASSESSMENT AND PAIN RELIEF
  2. CAUSE RELATED THERAPY (hygiene phase - prevention and OHI, non-surgical therapy - instrumentation)
  3. Re-evaluation & make corrective treatment plan
  4. definitive treatment (further non-surg tx?, local delivery anti-microbials, perio surgery)
  5. re-evaluation and maintenance (only for STABLE PERIO PATIENTS!!!!)
108
Q

What ultimately leads to TISSUE DESTRUCTION in the periodontium

A

how bacteria cause destruction vs the host destruction
enzymes, toxins, chemical messengers, acids etc - BOTH RESPONSES RELEASE THE SAME THING WHICH LEADS TO THE TISSUE DESTRUCTION

109
Q

A FULL perio exam is a more detailed assessment of disease extent and the info obtained can be used to:(6) points

A
  • determine a dx
  • educate the patient
  • inform treatment choice/make a treatment
  • monitor treatment outcomes
  • assess periodontal status and prognosis on an annual basis for pts with perio during MAINTENANCE THERAPY (who are stable)

It can also be used to show, from a medico-legal standpoint that you have recognised diagnosed and treated the condition appropriately

110
Q

Why is measuring BOP important

A

bleeding from the base of the pocket is measured and indicates that active, progressive disease may be present. - A RISK MARKER

111
Q

What do radiographs allow a clinician to assess (5)

A
  • root length and morphology
  • the level of alveolar bone and remaining bone support
  • the periodontal ligament space and PA region
  • furcation involvement of molar and premolar teeth
  • restorations/caries and sometimes subgingival calculus.
112
Q

WHY are PERIAPICALS considered the gold standard for periodontal assessment

A

they provide extensive information about the extent of bone loss, apical status of root, endo-perio lesions, root fractures, and deposits on root surfaces.

113
Q

What does a radiographic report include? (6)

A
  • the degree of bone loss - if the apex is visible this should be recorded as a percentage of the root surface affected
    -the type of bone loss - horizontal/vertical
  • distribution/extent of bone loss - localised or generalised
  • the presence of any furcation defects
  • the presence of subgingival calculus
  • other features including endo lesions, abnormal root length/morphology, overhangs, root fillings, caries.
114
Q

What are some other diagnostic tools we can use for perio disease

A
  • study models - digital or conventional - can be useful in the monitoring of gingival recession
  • clinical photos
115
Q

The aim of periodontal treatment is to: 5 points from SDCEP guidance

A
  • CONTROL patients symptoms
  • REDUCE inflammation
  • provide advice on risk factor control to reduce the risk of ongoing disease
  • STABILISE disease
  • support the patient AFTER treatment is complete to either limit further tissue loss or prevent further recurrence of disease.
116
Q

What is OH TIPPS

A

Modelled on Pt behaviour change strategies which have been shown to be effective at improving OH behaviour when carried out in PRIMARY CARE.

It aims to make the pt feel more confident in there ability to perform effective plaque biofilm removal, supports them to learn the manual skills and helps them plan how and when they will look after there teeth and gums.

117
Q

What does TIPPS stand for

A

t - talk
i - instruct
p - practise
p - plan
s - support

118
Q

What is important to consider when choosing the INTERPROXIMAL aid for mechanical plaque removal?

A

Consider:
- the size of the space
- the interdental papillae
- tooth anatomy
- patients ABILITY to carry out effectively

119
Q

Describe a study found that toothpaste can can actually remove plaque

A

De La Rosa 1979 studied brushing with and without toothpaste.
After brushing (WITHOUT TP), he found 60% plaque REMAINED
Regrowth was 27% LOWER in the group which used toothpaste due to bacteriostatic/cidal properties of fluoride - concluded that use of toothpaste is more effective

120
Q

What do we recommend to our patients regarding the ‘ideal toothpaste’

A

kids ages less than 3 = 1000ppm, smear
kids aged 3+ = 1350-1500 average recommendations

HIGH CARIES RISK (enhanced prevention) = over 10 = 2800ppm
over 16 = 5000

121
Q

What are the 3 theories of Progression (sokransky)

A
  • CONTINUOUS RATE THEORY
  • RANDOM BURST THEORY
  • ASYNCHRONOUS MULTIPLE BURST THEORY
122
Q

What occurs within the continuous rate theory? (3)

A
  • sites are either active or inactive
  • at ACTIVE sites the progression continues at a CONSTANT RATE over time, unless treatment is carried out
  • different active sites in a patient may be progressing at different rates (ie some faster than others)
123
Q

Describe what occurs within the random burst theory? (3)

A
  • AGAIN, sites can be either ACTIVE or INACTIVE
  • At active sites - there are random (episodic) bursts of perio destruction followed by periods of no activity with possible periods of repair
  • think - individual pockets in the mouth have different micro-environments due to different plaque levels, root anatomy, levels of calculus, diff bacterial profiles!
124
Q

Describe what happens within the asynchronous multiple burst theory? (2)

A
  • similar to random burst theory except that multiple active sites breakdown within a SHORT DEFINED period of time. ie maybe a period of ill health, stress or presence of various other risk factors!
  • Activity followed by long periods of no activity
125
Q

What is RAL

A

Rapid Attachment Loss - extensive loss of attachment detected in a SHORT period of time (pts with high susceptibility will tend to progress more with this)

126
Q

What is GAL

A

Gradual Attachment Loss - small amounts of loss of attachment over time either lots of mini-bursts or slow continuous loss of attachment
(patients with lower susceptibility will tend to progress more with this)

127
Q

What causes pregnancy - associated gingivitis ?

A
  • the changes in hormone levels (increase in estrogen and progesterone levels) and to the immune response associated with pregnancy have been shown there is a relation in the development/worsening of gingivitis
128
Q

What position should we lie a pregnancy patient on the dental chair?

A
  • important in 3rd trimester not to treat SUPINE
  • Correct positioning avoids maternal vena cava and aorta compression
  • RIGHT HIP ELEVATED !
129
Q

Can we place dental amalgam on a pregnant woman?

A

NO - it cannot be placed on the following people:
- children under 15 y/o
- pregnant women/breastfeeding
EXCEPT when deemed STRICTLY necessary by the dental practitioner based on the specific MEDICAL needs of the patient

130
Q

What is a chemical adjunct?

A
  • adjunct is a therapeutic intervention used IN ADDITION to operative perio therapy.
  • Can be divided into systemic adjuncts (systemic medications) and locally delivered adjuncts (delivered directly into the site of periodontal disease activity via the pocket!)
131
Q

What type of systemically delivered antibiotics can we get? - for chemical adjuncts

A
  • tetracycline
  • doxycycline - taken over a v long period of time as it is given in such a small dosage every 3, 6, 9, 12 months (perio sub-dose?)
  • metronidazole/ amoxycillin
132
Q

What types of locally delivered chemical adjuncts can we get ?

A

mainly ANTISEPTICS into perio pocket eg
- chlorohexidine mouthwash
- we can now use perio chips which we place directly into perio pocket which slowly dissolves over a longer period of time with an antibiotic within.

133
Q

what is the pattern of vibration of the PIEZO-ELECTRIC type of ultrasonic

A

The pattern of vibration of the tip is BACK AND FORTH with the 2 sides of the tip being ACTIVE

134
Q

what is the pattern of vibration of the magneto-strictive type of ultrasonic?

A

‘stack’ type of tip, current produces a MAGNETIC field which causes the tip to VIBRATE IN AN ELLIPTICAL pattern this means that all sides of the tip are active when applied to tooth.

135
Q

What are the different shapes of calculus that can be seen under the microscope ? 5 types

A

Brushite
Dicalcium phosphate dihydrate
Octacalcium phosphate
Hydroxyapatite
Whitlockite

136
Q

How can we prevent dentine hypersensitivity ? - 5

A

Instigate prevention
reduce dietary acid
advise patients not to brush teeth immediately after eating (this increases the amount of tooth surface abraded with TB)
wait ONE HOUR after brushing
show correct TBING method

137
Q

What can the treatment options be for dentine hypersensitivity - 4

A

prevention
remove cause if possible
OCCLUDE tubules topically - potassium ions - sensodyne, potassium oxalate
in extreme cases, we may need to revitalise the tooth ie rct

138
Q

What are the 7 IDEAL properties of a de-sensitising agent?

A

non-irritant to the pulp
relatively painless on application
easily applied
rapid onset of action
effective permanently
should not stain the teeth
CONSISTENTLY effective

139
Q

What 8 things should be kept in a patients notes/records?

A

histories/complaints
charts
attendance/non-attendance/cancellations
radiographs
clinical findings
record of treatment carried out
consent
referral letters

140
Q

How can we work out pack years ?

A

This is a way to measure the amount a person has smoked over a long period of time. It is calculated by :
multiplying the number of packs of cigarettes smoked per day by the number of years the person has smoked DIVIDED BY 20

141
Q

What are some contra-indications of using an ultrasonic

A

Patients with a pacemaker - electromagnetic waves from unit interfere with the electronic function of the pacemaker
Patients with contagious disease:
- hepatitis
- hiv/aids
- tuberculosis

142
Q

Why may it be difficult to achieve a good result after carrying out sub-gingival pmpr (7)

A
  • deep/tortuous pocket
  • poor access
  • furcation involvement
  • narrow embrasure/overcontoured restorations
  • tenacious calculus
  • non-ideal instruments
  • skill levels do not match the situation
143
Q

What is the evidence to show that RSD works?

A
  • doing RSD on a 4mm pocket does not improve perio pocket depths and can likely cause loa due to trauma.
  • pockets of 4-6mm show that there is a decrease by perio pockets depths of 1mm and an increase of 0.5mm attachment
  • over 6mm perio pockets we get a 2 mm reduction in pocket depth and 1mm
    = THE DEEPER THE POCKET THE MORE AN AFFECT WE WILL GET.
144
Q

WHAT IS YOUR PATIENTS PACK YEARS

A

2.5 YEARS

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