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FINALS EXAM FLASHCARDS > PERIODONTOLOGY > Flashcards

PERIODONTOLOGY Flashcards

1
Q

What are the two types of mechanical scalers used?

A

Ultrasonic - operating above 20kHz (kilohertz)
Sonic (or Air) - operating between 5-10kHz

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2
Q

What is the function of the mechanical scalers?

A

Both types of instrument use a water spray at the working tip. the water acts to cool the working tip (the tip becomes heated in use) and to flush debris away from the site of operation

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3
Q

Describe features of an ultrasonic

A

They operate at a frequency of between 20,000 and 30,000 vibrations per second (20-30 kHz)
They are NOT air driven but powered by an electric current
Far more effective and patient friendly than sonic scalers

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4
Q

Describe the Magnetostrictive type of ultrasonic

A

Magnetostrictive (think cavitron) - a stack of ferromagnetic metal is acted upon by electrical windings in the handpiece, which produce an alterning MAGNETIC movement. When the stack is magnetised it contracts and this movement is transferred to the working tip and tooth surface!

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5
Q

describe the pizoelectric type of ultrasonic

A

this is when small currents of electricity are used to alter the diamonds of quartz crystals on the working tip which produces vibration effect

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6
Q

Describe the MECHANICAL action of the ultrasonic

A
  • MECHANICAL - mixture of back and forth circulatory movements of the working tip mechanically abrades and chips away at the calculus deposits on the tooth surface.
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7
Q

describe the CAVITATIONAL effect that ultrasonics provide

A

the coolant water contains minute air bubbles which are expanded by the energy at the vibrating tip causing them to implode and release shock waves removing calculus and plaque biofilm
air bubbles also release oxygen which kills anaerobic bacteria within the periodontal pockets. v effective and vital use.

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8
Q

Describe the acoustic streaming action of an USS

A

All mechanical scalers set up vigorous movements of water around their tips known as acoustic streaming
helps to remove some of the tooth surface deposits and disrupt plaque colonies.

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9
Q

when would we consider using a mechanical scaler? (5)

A

supra/sub deposits
pre during and post sub ging PMPR
cavitational effect only
stain removal
removal of excess cement/amalgam ledges

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10
Q

What is the main potential hazard of using a mechanical scaler

A

From the clinicians POV, hazard is from the AEROSOL generated by the combined action of water spray and working tip. Most important that the clinician wears full PPE whilst carrying out this procedure.

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11
Q

When may we not use a mechanical scaler? (8)

A
  • porcelain jacket crowns can be fractured -best to avoid crowns when using USS here
  • hypersensitivity, decalcification, implants
  • pacemaker
  • COPD
  • very old/young
  • anxious patients
  • hypersensitivity - exposed dentine
  • decalcification - IRREVERSIBLE damage will occur
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12
Q

Describe the interference that an USS could have on a pacemaker.

A

Pacemakers and ICDs are sensitive to strong electromagnetic signals that may temporarily interfere with function.
Most devices are now designed with safeguards that include electronic FILTERS or SHIELDS that insulate the presence of electromagnetic interference.

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13
Q

What is the AIM of perio treatment

A

To reduce pathogens in the sub-gingival biofilm to a level which is conducive to healing.

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14
Q

What is dental calculus?

A

Hardened plaque by saliva
Acts as a rough surface which encourages further plaque accumulation (plaque retentive factor).
This is why removal of calculus is an essential element of perio treatment. it is very adherent to tooth surfaces and can only be removed by dental professional

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15
Q

Features of supra-gingival calculus (3)

A

Colour - yellow/brown
Heaviest opposite openings of salivary ducts (lingual lower incisors, buccal upper molars)
Fairly hard and brittle

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16
Q

features of sub-gingival calculus(5)

A

attached to root surfaces
colour - dark green/black
within perio pockets and not directly visible unless tissue shrinkage has ocurred
occurs throughout the mouth
very hard and can be difficult to remove with instruments

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17
Q

What instrument can we use to detect sub-ging calc

A

cross calculus probe to detect on root surfaces

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18
Q

Describe some features of the cross-calculus probe

A

double ended “hooked” instrument
place on tooth with the lower shank parallel to the long axis of tooth
with the hooked side facing the tooth, gently place instrument into the pocket
apply gentle pressure against the root surface an slowly with draw the probe out of the pocket. ledges of sub calc will be detected on root surface.

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19
Q

List some advantages of powered scalers (6)

A
  • simple and effective - less time than hand scaling
  • can be used supra/sub
  • no instrument sharpening required
  • water spray provides constant lavage and irrigation
  • useful in tight pockets as less tissue distortion
  • useful for furcations
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20
Q

What is reattachment of the periodontium?

A
  • describes reunion of root and connective tissue seperated by incision or injury
  • re attachment of epithelium in perio disease does NOT occur, therefore, reattachment is not a term we use when we refer to PERIODONTAL HEALING.
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21
Q

What is NEW attachment

A
  • describes union of connective tissue with previously pathogenically ALTERED root surface.
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22
Q

Describe the effects of mechanical plaque control on the microflora (subgingival PMPR) (4)

A
  • there is a marked decrease in the total number of organisms (regardless of type)
  • the proportion of gram-ve anaerobic (main cause of perio disease) organisms is greatly reduced
  • residual flora is gram positive aerobic
  • these changes in sub-gingival plaque flora are partly due to a reduction in plaque thickness - less MOTILE bacteria
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23
Q

Following RSD treatment, what do we typically see…

A
  • there is an initial ACUTE inflammatory reaction as a result of trauma - begins to subside after 24-48 hours
  • over following week post rsd we should see decrease in vasodilation, GCF, PMN’S, ulceration of pocket
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24
Q

over time, what can we then see post sub-ging PMPR in healing of the perio tissues (3)

A
  • fibroblasts migrate to the site and collagen fibres are laid down. elasticity in epithelium return. (FIBROBLASTS PRODUCE COLLAGEN)
    -limited re-modelling of the alveolar crest takes place (bone doesn’t regrow in perio treatment! )
    -pocket epithelium begins to attach to root surface (attaches via hemi-desmosomes)
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25
Q

Describe how the pocket epithelium begins to attach to the root surface (5)

A
  • New attachment is known as the long junctional epithelium (JE). It attaches by hemi-desmosomes to make a desmosome.
  • The junctional epithelium migrates apically resulting in a loss of the PDL
  • no gingival fibres involved. gingivae attaches directly to the root surfaces. LONG JUNCTIONAL EPITHELIUM.
  • healing is via the basement of a membrane.
  • THIS IS A MUCH MORE FRAGILE ATTACHMENT this is why we cant probe…
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26
Q

What happens during NEW ATTACHMENT POST sub-ging PMPR

A

there is formation of the LONG JUNCTIONAL EPITHELIUM
this long epithelium results in gradual closure of a pocket and may continue for months after treatment
think of the junctional epithelium acting like a zip/zips up pockets

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27
Q

What will we see CLINICALLY during the healing process of sub ging pmpr to see if tx has been a success or not? (5)

A
  • Initially, a reduction in redness and swelling as the inflammation subsides
  • BOP is reduced as inflammation resolves
  • Ulcers in pocket epithelium heal
  • Gingivae become increasingly pink and firm as connective tissue matures
  • As inflammation subsides there is SHRINKAGE of the tissues (gingival shrinkage)
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28
Q

What are some cons (disadvantages) to gingival shrinkage as a post op symptom from subging pmpr

A
  • can expose dentine and lead to dentine hypersensitivity
  • pts not aesthetically pleased sometimes
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29
Q

What is gingival shrinkage due to?

A

due to a tightening in the gingival CUFF

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30
Q

What is released during healing of sub ging pmpr

A

CYTOKINES are released during healing which have a regulatory function !
proliferation and healing of the ulcerated pocket is stimulated by cytokines, which in turn attract fibroblasts. (FIBROBLASTS PRODUCE COLLAGEN)

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31
Q

What are cytokines in perio healing

A

a group of proteins that are released to trigger a certain amount of processes eg attracting fibroblasts, neutrophils etc.

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32
Q

what is regeneration in perio healing?

A

this means the attachment of PDL cells and fibres to new cementum formation and coronal regrowth of alveolar bone (IDEAL AIM IN PERIO TREATMENT IS TO PROMOTE COMPLETE PERIO REGENERATION)

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33
Q

Why to bone cells and periodontal ligament cells NOT regenerate?

A

Because they are much more COMPLEX cells than simple epithelial cells. they take a lot more time to reproduce and are never given a chance to regenerate.

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34
Q

list some of the periodontal surgery techniques used to PROMOTE NEW ATTACHMENT

A

bone grafting
conditioning of root surfaces
use of membranes

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35
Q

Describe what guided tissue regeneration is (3)

A
  • currently most successful method of new attachment formation
  • uses mechanical barrier to eliminate epithelium from wound to determine which cells repopulate wound
  • promotes population by cells derived from PDL and bone
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36
Q

List some of the future prospects for managing perio disease (4)

A
  • prevention of the disease
  • diagnostic testing
  • chemotherapy
  • new attachment (guided tissue regeneration)
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37
Q

what is RECESSION (3)

A
  • a seemingly inflammation-free clinical condition characterised by apical retreat of the periodontium
  • THE ID PAPILLA OFTEN REMAIN AT THE NORMAL LEVEL
  • teeth are never lost due to true recession
    recession can be localised or generalised
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38
Q

2 terms to do with gingival recession:
what do we mean by FENESTRATION?

A

this is a WINDOW in the bone, usually found on the buccal aspect in patients

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39
Q

what do we mean by DEHISCNECE

A

this is a LACK of bone, commonly where a tooth is proclined. happens commonly on lower anterior area

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40
Q

list some of the different reasons for recession (5)

A
  • chronic minor trauma eg improper tooth brushing technique
    -mild chronic inflammation
    -frenum pulls
    -ortho treatment
    -excessive perio scaling
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41
Q

Describe what we should look for clinically when looking at recession. (4)

A
  • stillmans clefts ‘v’ shape in gum
  • mcCall’s festoons - gum has a rolled margin
  • clinical recessions
  • RADIOGRAPHS DO NOT AID DIAGNOSIS
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42
Q

List some of the problems associated with recession (3)

A
  • dentine hypersensitivity
  • root caries (as more of root is exposed)
  • toothbrush abrasion
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43
Q

what is localised recession usually caused by?

A

usually seen on lower ants, due to fraenum pull, thin buccal bone covering

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44
Q

list some of the ways we can monitor recession (3)

A

clinically measure - LOA/pocket depths
clinical photographs
study models (3D record of the mouth)

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45
Q

list some of the treatment options for recession (3)

A

firstly, eliminate any casual factors
- modify brushing technique
- eliminate areas of mild chronic inflammation eg replace faulty restoration margins
- frenectomy for anteriors ie localised recession

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46
Q

Describe what furcation involvement is

A

this is the HORIZONTAL loss of support in areas where roots of MULTI-ROOTED teeth converge.

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47
Q

How can we diagnose a pt with furcations

A

these are diagnosed via radiographic AND clinical examinations (not just off a radiographic report alone)
radiographs suggest where they may be.
clinical examinations confirm if they are present or not.
IT NOT EXPOSED IN MOUTH IT IS NOT A FURCATION - needs to be verified clinically - as with everything eg caries, restorations etc

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48
Q

What is the index called that we use to measure furcation involvement in the mouth

A

HAMP ET AL
Grade 1 - horizontal loss of support. less than a 3rd of the way through
Grade 2 - horizontal loss of support. more than a 3rd of the way through
Grade 3 - ALL the way through

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49
Q

Why should we be worried about a furcation involvement on a tooth (3)

A

due to it REDUCING THE PROGNOSIS of a tooth. There are 2 reasons:
1. Furcations are more difficult to clean hence less control of disease as hard to clean
2. Loss of vitality of the tooth may occur due to accessory canals running from the pulp chamber into the furcation area act as a stagnation area for bacteria etc.

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50
Q

Because of the reduced prognosis of furcation involved teeth, what should we carry out at regular intervals

A

VITALITY TESTING

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51
Q

What are the treatment options for furcation involvement

A

either to expose the furcation for access for easier cleaning or to induce regeneration of new bone ie guided tissue regeneration

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52
Q

What are the treatment options for a grade 1 furcation

A

scale/polish, RSD/PMPR, OHI
furcationplasty - where a bur is used to widen the lesion reshaping it making it easier to clean.

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53
Q

list some of the treatment options of a grade 2 furcation (5)

A
  • furcationplasty
  • tunnel preparation (open all the way up and make it a grade 3 through-through)
  • guided tissue regeneration
  • root resection - where one root is cut off and removed so we have no furcation lesion left to worry about - making it a single root.
  • tooth XLA due to poor prognosis
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54
Q

treatment options for a grade 3 furcation (3)

A

tunnel prep
root resection
tooth xla

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55
Q

what is the BEST treatment for a furcation involvement on a tooth (4)

A

GOOD OH
- make pt aware of where furcation involvement is
- explain why important to pay particular attention to this area
- use single tufted toothbrushes etc.

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56
Q

Describe the chemical composition of dentine

A

70% inorganic (hydroxyapetite crystals)
20% organic (collagen)
10% water

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57
Q

What does dentine contain?

A

collagen, mucopolysaccharide ground substance processes of the odontoblasts

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58
Q

where to the odontoblasts lie in dentine

A

PERIPHERY OF PULP - while their processes extend from their cell bodies to the amelo-dentinal junction

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59
Q

what is the function of dentine tubules

A

the dentinal tubules allow passage of fluid, chemical agents and bacteria

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60
Q

What is secondary dentine?

A

Describes the dentine that is produced AFTER the tooth has become fully formed. it is formed slowly throughout life preferentially deposited on the floor and roof of pulp chamber.

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61
Q

What is tertiary dentine

A

this is produced when the dentine is in contact with a noxious stimulus such as caries or tooth surface loss
odontoblasts lay down more dentine

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62
Q

is dentine highly innervated

A

YES

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63
Q

what is the definition of dentine hypersensitivity

A

pain arising from exposed dentine typically in response to chemical, thermal or osmotic stimuli that cannot be explained as arising from any other form of dental defect or pathology.

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64
Q

Where do we get most sensitivity from in a tooth

A

it is more sensitive at the dentinoenamel junction and close to the pulp. if the pulp is inflamed, the dentinal sensitivity is increased (even only slightly)

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65
Q

How can we treat dentine hypersensitivity? (5)

A

PREVENTION FIRST
REMOVE CAUSE IF POSSIBLE
Occlude tubules topically eg sensodyne (potassium ions)
Insulative restoration (protect the tubules from being exposed)
May have to DEVITALISE TOOTH eg RCT

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66
Q

How can we prevent dentine hypersensitivity from happening in the first place? (4)

A

INSTIGATE PREVENTION!
- REDUCE DIETARY ACID!
- advise pts not to brush teeth immediately after brushing (increases amount of tooth surface abraded with tooth brush - wait an hour)
- show pt correct brushing method

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67
Q

List the ideal properties of a desensitising agent: (7)

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
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68
Q

list the 7 desensitising agents (7)

A

sodium fluoride
stannous fluoride
sodium monofluorophosphate
calcium hydroxide
strontium hydroxide
formaldehyde
resins and adhesives

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69
Q

List some properties of sodium fluoride (3)

A

fluoride from sodium salt is taken up into dentine making it more resistant to acid decalcification
Possible increase in secondary dentine formation which will block dentinal tubules
MUST be applied frequently for benefit!
can be found in paste, gels, mouthwashes (THINK DURAPHAT)

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70
Q

What is sodium monofluorophosphate used in?

A

TOOTHPASTE (fluoride salt)

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71
Q

What is the role of calcium hydroxide? (2)

A

sometimes used as a LINING for fillings, occludes dentinal tubules but adheres POORLY to dentine therefore uncertain efficacy

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72
Q

How does Seal&Protect work?

A

Mechanically blocks OPEN dentinal tubules on root surface, contains fluoride and triclosan
is a resin and is light cured

73
Q

What are the 5 phases of treatment planning for a patient with periodontal disease.

A
  1. Initial examination and pain relief
  2. cause related therapy (4 sub groups)
  3. re-examination/assessment (allow 10-12 weeks after last sub ging pmpr session , repeat 6ppc)
  4. Definitive treatment plan
  5. MAINTENANCE /supportive perio therapy/care
74
Q

What is the GOAL of non-surgical therapy for a perio patient? in other words - goal of RSD

A

render the roots biologically compatible with soft tissue by eliminating calculus and altered cementum and reducing perio pathogenic micro-organisms

75
Q

Describe the 3 objectives of cause-related therapy

A

to resolve the disease process
to create conditions that will mitigate against recurrence of the disease
- involves controlling dental plaque supra/sub-gingivally.

76
Q

What are the clinical considerations that we can take into account regarding cause related therapy ?

A
  • caries ?
  • restoration overhangs/deficiences?
  • furcation involvement
  • sensitivity testing
  • occlusal trauma
  • mobility
77
Q

What are some areas of advice we can give patients? (6)

A

OHI
Denture hygiene
Smoking cessation
Alcohol reduction
Dietary advice
Dentine hypersensitivity

78
Q

List the options of non-surgical therapy treatment we provide as therapists; (6)

A
  • correction of faulty rests margins
  • scaling and polishing
  • RSD
  • treatment of furcation involvements
  • treatment of dentine hypersens’
  • XLA of teeth with poor prognosis
79
Q

What is involved in the re-examination (phase 3) part of a treatment plan? (3)

A
  • this is necessary to determine the patients response to treatment
  • evaluation of both the tissue response and pts co-operation now possible
  • re-evaluation should be much more accurate than the initial exam.
80
Q

if the perio treatment outcome for a pt is a success, what then happens?

A

the patient should progress directly to maintenance or supportive therapy
this is NECESSARY as the patient is NOT cured and recurrence is likely if plaque levels rise above the disease threshold
ONCE A PERIO PATIENT ALWAYS A PERIO PATIENT

81
Q

if the perio treatment outcome fails for a patient, what does this then mean/lead to?

A
  • firstly, establish the cause(s) of failure - there are many causes but the most likely is inadequate OH
  • if the cause can be corrected, further treatment may be given with the intent of achieving treatment success!
  • if the cause cannot be correct, the patient goes to PALLAITIVE care.
82
Q

What is palliative care for a perio patient?

A

this is NOT the same as maintenance - maintenance is a recall system for patients once their disease is STABILISED
it is designed to try and maintain DISEASE STABILITY.

83
Q

What is the MAIN AIM of palliative care?

A

to SLOW disease down while attempting to keep the patient comfortable with a functioning dentition

84
Q

what does the treatment involve for a palliative care patient?

A

it is very simple, - an S&P every 2/3 months

also, we would advise the patient that in the event of a problem arising with a tooth on palliative care ie excessive mobility, abscess - XLA MAY BE THE ONLY OPTION

85
Q

What are the different phase 3 outcomes? (3)

A
  • Currently Stable = BOP is less than 10%, PPDs are less than or equal to 4mm with no BOP at 4mm sites!
  • currently in remission = BOP is more than or equal to 10%, PPDs are less than or equal to 4mm with no BOP at 4mm sites
    2 ABOVE IS WHERE PTS CAN PROGRESS TO MAINTENANCE (phase 5) OR:
  • currently unstable = PPDs are more than or equal to 5mm or PPDs are more than or equal to 4mm with BOP.
    THESE PATIENTS PROGRESS TO PHASE 4 - DEFINITVE TREATMENT.
86
Q

What is the treatment involved in Phase 4 for a patient?

A

RSD
perio surgery - depends on findings at the re-examination phase
endo treatment
definitive restorative and pros treatment
PATIENTS CAN ONLY PROGRESS ONTO PHASE 5 ONCE THE PERIODONTIUM IS STABLE - if not, palliative care.

87
Q

What is involved in phase 5 of perio treatment? (4)

A
  • a recall system which attempts to maintain perio stability!
  • general and local risk factors will affect recall times (recall times are usually short to keep maintenance up to a high standard. )
  • recurrence of disease will mean that patients return to other treatment phases
  • RE-STABILISATION LEADS BACK TO MAINTENANCE !
88
Q

What is a periodontal pocket and what does it involve?

A

a pathologically deepened gingival crevice, the pocket involves the ulcerated epithelial lining of the pocket wall, the JE, the diseased root surface which is contaminated with subging calc deposits and a layer of dental plaque - THIS CONTAINS PERIO PATHOGENS

89
Q

What is the AIM of perio treatment

A

to create an environment that is biologically compatible with healing of the periodontal tissues, We do this by decontamination of the root surface, disruption and elimination of the plaque biofilm on the root surface, removal of bulk subgingival calculus from the root surface

90
Q

What is RSD

A

this describes the procedure that is necessary to eliminate or disrupt the endotoxins from the anaerobic plaque bacteria

91
Q

why is it important to eliminate calculus from the dentition

A

all calc has a coating of dental plaque
supra calc impedes both tbing and id cleaning
subging calc may absorb bacterial endotoxins
may impede perio probing thereby giving false ppds

92
Q

How to pockets heal following perio treatment

A

pockets heal by resolution of inflammation and the formation of the long JE - DEEP POCKETS SHOW GREATER REDUCTION OF PROBING DEPTHS FOLLOWING TREATMENT THAN SHALLOW POCKETS!

93
Q

List the 8 stages of cause related therapy

A
  • treat any acute/painful condition
  • hygiene phase therapy
  • smoking cessation
  • removal of any plaque retentive factors
  • supra scaling (removal of plaque and calculus)
  • subging scaling/RSD (most conservative method of pocket reduction)
  • occlusal adjustment if necessary
  • monitor initial response to therapy
94
Q

list some plaque retentive factors we may have (3 main ones)

A

restoration deficiencies ledges, faulty appliances eg dentures/ortho appliances, crowns and bridges

95
Q

Why is subgingival calculus hard and tenacious

A

Due to the filamentous bacteria which can penetrate into surface cementum

96
Q

Another aim of RSD in perio pockets is to:

A

REMOVE VIRULENT gram negative anaerobic bacteria (most destructuve)

97
Q

What pieces of information do we need to formulate a periodontal treatment plan? (3)

A

Patient history
Examination (including perio exam)
Further/special investigations etc

98
Q

What do we do if we have a BPE code 3 with evidence of ID recession? (LOA)

A

treat as a code 4! due to the ID recession

99
Q

What are the 4 sub-sections that case related therapy can be divided into

A
  1. clinical checks (caries, overhangs, furcations, sensitivity testing etc)
  2. discussion of disease with patient (important part of patient informed consent for treatment!)
  3. advises (OHI, smoking cessation, alcohol reduction, diet advice etc)
  4. debridement
100
Q

What does the discussion of perio disease with the patient involve? (4)

A

Discussion of the nature and treatment of perio disease
Perio diagnosis
Treatment options available
Importance of the patients part in managing risks factors eg plaque control

101
Q

What does debridement (sub-stage 4 of case related therapy) involve? (4)

A

Active treatment in order to attempt to stabilise disease, which may include :
- XLA
- removal of overhands/deficiencies (where plaque can attract to )
- supra/sub ging scaling
- management of active caries etc.

102
Q

List some features of a healthy periodontium (5)

A

Pink/racial pigmentation
stippled: orange peel appearance
knife-edge margin to the tooth (ID papillae)
Papillae exactly fill the ID space
No BOP from the BASE of the pocket

103
Q

List some features of an unhealthy periodontium (6)

A

red swollen/inflammed gingiva with:
- loss of knife-edge margin
- papillae over or under-fill the ID space
- loss of stippling
- BOP from the base of pocket (this means there is evidence of active disease at the site at that time)
- these can be clinical features of either gingivitis or perio

104
Q

Is there LOA in gingivitis ?

A

NO - base of pocket is at coronal (above) the Amelocemental Junction (ACJ)
- FALSE POCKETS
- this condition is reversible (no permanent damage)

105
Q

What is the small groove between the gingival margin and the tooth enamel?

A

gingival sulcus/gingival crevice

106
Q

What can happen in the gingival sulcus/gingival crevice ?

A

plaque biofilm can quickly develop at the gingival margin following OH or supra cleaning and over time will enter the gingival sulcus

107
Q

What is found at the BASE of the gingival sulcus?

A

the JUNCTIONAL EPITHELIUM - this has wide spaces between the epithelial cells allowing plaque bacteria and toxins to leak into the underlying gingival connective tissue causing inflammation

108
Q

list the main problem of the junctional epithelium

A

It is the weak point in the gingival barrier against invading plaque bacteria.

109
Q

List the two ‘types’ that histological clinical gingival health can be split up into

A

pristine gingival health (LONG TERM excellent oral hygiene) - this is v rare
Clinically healthy gingiva : adequate levels of oral hygiene - MAINTANED
these 2 categories clinically both look virtually the same (healthy gingiva)

110
Q

describe what happens HISTOLOGICALLY in clinical gingival health

A

LOW LEVELS OF INFLAMMATORY INFILTRATE
(many neutrophils and some B cells lymphocytes) - this is all underlying the junctional epithelium. (so even though clinically the gingiva appears healthy , HISTOLOGICALLY there is always an inflammatory reaction to plaque bacteria)

111
Q

What does the ongoing low level inflammatory reaction in the connective tissue (under the JE) result in?

A

the formation of (gingival crevicular fluid) GCF

112
Q

What is GCF?

A

a serum-like fluid formed from the post-capillary venules of the dentogingival plexus

113
Q

What is the dentogingival plexus

A

a dense network of blood vessels in the gingival connective tissue sub-adjacent to the JE

114
Q

what makes up (components) GCF

A

various plasma proteins
defence cells/proteins (neutrophils - PMNs antibodies, complement - these help to combat the potentially invading plaque bacteria)
growth factors

115
Q

What is the periodontium

A

a set of specialised support structures and tissues within the jaws, surrounding the teeth. the periodontium is richly innervated by nerve fibres and blood vasculature. the trigeminal nerve (CN V) provides sensory and autonomic innervation to the periodontium through the periosteum both in the maxilla and mandible through its branches.

116
Q

What makes up the periodontium

A

3 components:
- bone
- gingivae
- pdl (periodontal ligament)

  • cementum (lines the root surface) - present on surface of roots of teeth (a dental hard tissue but considered as part of the periodontium)
117
Q

What are the teeth attached to the alveolar bone by?

A

small fibres of the PDL - known as sharpeys fibres connecting via the cementum

118
Q

describe the ‘makeup’ of alveolar bone

A

contains lost of spaces and known as cancellous or trabecular bone - has a spongy appearance

119
Q

how can we see the lamina dura on a radiograph

A

seen as a radiOPAQUE which identifies the cribiform plate

120
Q

what are the gingival tissues made up of (2)

A

the ATTAHCED and FREE gingiva
Alveolar mucosa

121
Q

What is the BPE used for/what tool do we use for this.

A

a SCREENING tool used to identify those individuals who require a more detailed perio examination (do not measure pockets with BPE probe)
we use a WHO probe - ball ended 0.5mm in diameter, coloured band from 3.5mm - 11.5mm, second coloured band 8.5-11.5mm
PROBING FORCE OF 20-25G

122
Q

describe the 5A’s for smoking cessation

A

Ask patient if they use tobacco (how long/how many) - can give us pack years!
Advise on the benefits of quitting (dental relevance ie perio disease etc, caries, ulceration due to dry mouth also)
Assess willingness (readiness) to quit RECORD THIS IN THE NOTES!
Assist in quit attempt! eg NRT or refer to counselling
Arrange follow up dental appts ask and praise each visit - makes the difference!

123
Q

describe the 5R’s regarding smoking cessation

A

Relevance
Risks
Rewards
Roadblocks
Repetition

124
Q

In which case would we use the 5R’s regarding smoking cessation for a patient?

A

the 5R’s are used when a patient is not yet in a place where they are ready to stop
the AIM is to provide motivation for them to potentially stop.

125
Q

What is brief intervention in smoking cessation? (3 main points to explain)

A

this is a opportunistic way of approaching smoking cessation advice - almost a casual reference (no more than 5 mins, not coming across as a threat) - PLANTING A SEED
a dental surgery provides the perfect setting to provide a brief intervention
evidence suggests that brief interventions in the dental surgery can be VERY effective at smoking cessation!

126
Q

What aids are available to stop smoking? (2)

A
  • NRT (nicotene replacement therapy)
  • non-nicotene products
127
Q

What do we mean by a ‘risk marker’ in perio disease? (2)

A

this implies the presence of disease but is NOT the cause of disease eg BOP indicates ACTIVE gum disease but is not the cause of the disease, same with tooth mobility

128
Q

What do we mean by a risk factor in perio disease?

A

this is a factor which INCREASES THE PROBABILITY that a disease may develop in an individual (risk factors are biologically related to the occurrence of the disease)

129
Q

name the 2 different types of risk factors in perio

A

LOCAL (‘local’ to the oral cavity and factors which may influence plaque accumulation)
SYSTEMIC (the HOST response)

130
Q

What can local risk factors be broken down into?

A

Anatomical risk factors
Latrogenic risk factors
Trauma from occlusion

131
Q

Describe anatomical risk factors (sub term from LOCAL risk factor) (4 main anatomical risk factors)

A

Furcation involvement - horizontal loss of support in areas where roots of multi-rooted teeth converge, these areas are difficult to access and clean.

Root morphology - root grooves are associated with localised deep, narrow pockets that do not respond to SUB
PMPR (usually upper lateral incisors)

Localised gingival recession - associated with - toothbrush trauma, high frenal attachment, habits, piercings, bony dehiscence’s

Dental anatomy and tooth arch relationships

132
Q

Describe the iatrogenic risk factors (2nd sub term from LOCAL risk factors) - 5 iatrogenic factors

A
  • overhanging restoration
  • poorly designed partial dentures
  • ortho appliances
  • defective crown margins
  • defective bridge pontics
133
Q

List the 6 SYSTEMIC risk factors relating to perio disease

A
  • genetic/inherited/inborn factors
  • environmental risk factors
  • behavioural risk factors
  • life-style risk factors
  • metabolic risk factors
  • haematological risk factors
134
Q

What is the management of systemic risk factors?

A

we must FIRST identify:
- thorough history, PMH and examination!
- specifically note any family history, smoking history, diabetic status.

135
Q

What are some genetic factors that could increase someones succeptibility for perio disease (3)

A
  • Down’s syndrome
  • chronic granulomatous disease
  • ehlers-danlos syndrome (defects collagen synthesis associated with hyper-extendible skin, hyper-mobility of joints and sever perio destruction!)
136
Q

What are some ENVIRONMENTAL risk factors relating to perio (a sub-category from the 6 systemic risk factors)

A

-drugs
eg anti-epileptics like phenytonin leading to gingival overgrowth, calcium-channel blockers, immunosuppressants

ANY OF THESE DRUGS can cause gingival overgrowth, false pocketing and subsequently true pocketing

137
Q

Name the 2 MOST IMPORTANT behavioural risk factors regarding perio (sub-category from 6 systemic risk factors)

A

POOR ORAL HYGIENE
SMOKING

138
Q

Describe typical things we can see in smokers (systemic, behavioural risk factor for perio disease)

A

smokers have:
- more sites with deep pockets
- more LOA and bone loss
- higher prevalence furcation lesions
- accumulate more calculus
- show LINK between ‘pack years’ (crude indicator of tobacco consumption)

139
Q

How do we work out pack years?

A

NO. of packs per day ‘x’ NO. of years the patient has smoked.

140
Q

What are the 6 stages of behavioural change in smokers

A

Pre-contemplation (not ready)
Contemplation (getting ready)
Preparation
Action
Maintenance
Termination

141
Q

What are some of the life-style risk factors relating to perio (one of the 6 systemic risk factors)

A
  • stress (reducing immune function, salivary production favouring increased plaque production)
  • malnutrition (individual vitamins can have an impact on the periodontium)
142
Q

What are some Metabolic risk factors relating to perio? (one of the 6 systemic risk factors)

A
  • diabetes
  • pregnancy and oral contraceptive
  • chron’s dosease
  • sarcoidosis
143
Q

Describe how diabetes relates to perio disease (3)

A
  • we have type 1 and type 2
  • the greater the systemic complications of diabetes, the more severe the periodontitis is!
  • the relationship between diabetes and plaque appears independent.
144
Q

What are some factors that can contribute to the risk in diabetic patients

A
  • PMNL function - may be genetically inherited or due to hyperglycaemia
  • collagen metabolism - less collagen synthesised
  • wound healing - decreased in diabetics
145
Q

How does pregnancy affect the periodontium ? (2)

A
  • PREGNANCY - if good OH, no problems, will exaggerate pre-existing gingivitis - increased response to inflammation due to progesterone.
  • OCP - progesterone containing, effects exaggerate a pre-existing gingivitis
146
Q

Describe the characteristics of a SUPRA-gingival plaque community (7)

A
  • oxygen levels vary
  • variable conditions (moisture/osmotic pressure, temperature, shear forces)
  • saliva
  • dietary carbohydrates
  • gram +ve DOMINATE
  • gram -ve increase with plaque layers (pellicle, more motile etc)
  • FACULTATIVE ANAEROBES DOMINATE (can survive in aerobic and anaerobic conditions)
147
Q

Describe the characteristics of a SUB-gingival plaque community (7)

A
  • Anaerobic
  • Constant conditions
  • Gingival crevicular fluid
  • proteins derived from serum
  • gram +ve DOMINATE
  • Gram -ve more abundant
  • OBLIGATE ANAEROBES (GNABs)
148
Q

What bacteria would we find with patients that have chronic perio?

A

Porphyromonas gingivalis
Fusobacterium nucleatum
tanerella forsythia
treponema denticola

149
Q

What bacteria would we find in patients with RAPIDLY progressive perio?

A

Porphyromonas gingivalis
Prevotella intermedia
fusobacterium nucleatum

150
Q

Describe socransky’s study (1998) regarding perio

A

5 clusters:

Red - DEEP PERIO POCKETS
Orange - DEEP PERIO POCKETS
Yellow
Purple
Green

151
Q

What bacteria are involved with the Red complex regarding socransky’s study?

A

Porphyromonas Gingivalis (black pigmented bacteria GNAB)
Tannerella forsythia (GNAB)
Treponema Denticola (spirochete, highly proteolytic)

152
Q

What bacteria are involved in the Orange complex?

A

Fusobacterium spp
Prevotella nigrescins
Prevotella intermedia

153
Q

What is the main bacteria that causes NUG?

A

TREPONEMA VINCETIL

154
Q

What are some of the disadvantages of using a BPE (8)

A
  • Lack of detail within sextants
  • Lack of information on actual disease activity
  • No information on LOA
  • Does not differentiate between true and false pockets
  • Lack of furcation involvement detail - NO info on severity
  • Cannot be used for young individuals as full clinical crown length maturation not occurred
  • cannot be used to monitor disease
  • required specialised probe
155
Q

What teeth do we probe when screening for a child (BPE)?

A

only 6 teeth checked - UR6, UR1, UL6, LL6, LL1, LR6

156
Q

Why do we measure BOP

A

the best indicator of active disease
use the probe in a gentle walking motion around the tooth

157
Q

Describe the 3 theories of progression that Socransky proposed.

A

Socransky et al (1984) proposed 3 different models to describe possible patterns and rate of progression of perio:
- CONTINUOUS RATE THEORY
- RANDOM BURST THEORY
- ASYNCHRONOUS MULTIPLE BURST THEORY

158
Q

Describe the Continuous rate theory

A
  • Sites are either ACTIVE or INACTIVE
  • At active sites, the progression (perio destruction) continues at a constant rate over time, unless treatment is carried out.
  • Different active sites in a patient may be progressing at different rates.
159
Q

Describe the random burst theory

A
  • Again, sites can be active or inactive
  • At active sites, there are random (episodic) bursts of periodontal destruction followed by periods of no activity with possible periods of repair
  • THINK - individual pockets in the mouth have different micro-environments due to diff plaque levels, root anatomy etc. some sights may have more virulent bacteria!
160
Q

Describe the Asynchronous Multiple Burst Theory

A
  • Similar to random burst theory, except that multiple active sites breakdown within a short defined periods of time: some transient factor causes multiple sites to breakdown at the same time eg period of ill health.
  • activity followed by long periods of no activity (quiescence)
161
Q

What are the two types of perio disease progression that have been detected in patients? (RAL AND GAL)

A

RAL - rapid attachment loss - extensive loss of attachment detected in a short period of time (detected by manual perio probes)
GAL - gradual attachment loss - small amounts of loss of attachment over time either in lots of mini-bursts or slow continuous loss of attachment (only detectable by very sensitive electronic probes etc)

162
Q

As plaque biofilm accumulates/matures, evidence of what is present, that we can see clinically and at a histological level? (5)

A
  • evidence of gingival inflammation increases with evidence of:
  • increased GCF flow
  • increase in inflammatory and immune cellular infiltrate in the connective tissue underlying the JE
  • Fewer fibroblasts in the gingival connective tissue underlying the JE
  • reduction in collagen content in the inflamed connective tissue under the JE.
163
Q

Describe the Page and Schroeder theory

A
  • This is a KEY publication which classified the histopathological changes which take place during the progression from gingivitis to periodontitis!
  • DIVIDED progressing lesion into 4 PHASES:
    1. initial lesion
    2. early lesion
    3. established lesion
    4. advanced lesion
164
Q

What can we see (clinically) in the initial and early lesions ?

A

early stages of gingivitis (no clinical signs)

165
Q

What can we see (clinically) with an established lesion?

A

clinically obvious gingivitis

166
Q

what can we see (clinically) in an advanced lesion?

A

periodontitis

167
Q

what occurs within the initial lesion phase? (5)

A
  • occurs within 24-48 hours of plaque accumulation
  • plaque mainly gram pos aerobic bacteria
  • vasodilation of blood vessels, increased no of neutrophils and increased GCF production .
  • tissue damage minimal
  • bacterial factors/antigens initiate an inflammatory/immune response
168
Q

what occurs within the early lesion? (8)

A
  • occurs after approx a week
  • immunoglobulin production and cytokines released
  • increase in size of inflammatory infiltrate
  • loss of fibroblasts and collagen in infiltrated area
  • increased GCF production
  • PMNs accumulate in gingival crevice.
  • due to the inflammatory swelling of the gingivae, this results in a deeper gingival crevice
  • favours the growth of gram neg bacteria associated with the release of endotoxins and enxymes which causes more tissue damage
169
Q

What occurs in the established lesion? (7)

A
  • this stage corresponds to clinically he diagnosis of gingivitis
  • gingival connective tissue largely replaced by inflammatory infiltrate.
  • JE replaced by ulcerated pocket epithelium
  • pocket epithelium is no longer attached to the tooth allowing APICAL migration of the crevice/pocket and plaque biofilm.
  • large numbers of PMNs espesh in the pocket epithelium
  • increased compliment and immunglobulins
  • bacterial products cause damage
170
Q

What occurs in an advanced lesion? (6)

A

inflammatory infiltrate extends apically and laterally
- continued loss of collagen
- ulceration and migration of junctional epithelium apically onto root surface
- THIS STAGE CORRESPONDS TO PERIODONTITIS
- there is an advancing inflammatory front where the host attempts to prevent the spread of the invading bacteria
- the apically advancing perio pocket created the ideal environment for the growth of the perio pathogens (gram neg anaerobes = gnabS)

171
Q

What is the role of the host response in the pathogenesis of perio disease (2)

A

Host response to plaque biofilm has two purposes :

  1. Protection of the host against local microbial attack
  2. prevention of spread of micro-organisms if manage to invade tissue
172
Q

Describe the tissue damage that happens with patients with perio

A
  • Destruction of PDL fibres inserting into the bone and cementum
  • loss of extracellular matrix ECM
  • fibroblasts damage
  • loss of the surface layer of cementum
173
Q

What is bone resorption in perio mediated by?

A

both host-derived and bacterial factors

174
Q

What is the main bacteria that causes NG

A

Treponema vincetil

175
Q

What are the clinical signs and symptoms of NG (6)

A

Pseudomembranous sluff - grey sluff
‘punched out’ papillae
bleeding/swollen/red
feotorous breath
general malaise
lymphadanapothy

176
Q

What are the pre-disposing factors of NG

A

smoking, stress, immunosuppression, poor OH

177
Q

How can we treat NG (5)

A

Metronidazole 500mg for 3-5 days
USS scale - cavitational effect breaking bacterial barrier (sub-gingival live anaerobically so O2 will disturb this)
OHI
smoking cessation
review once course of ABs has finished

178
Q

List the different types of perio surgery we can carry out (6)

A
  • gingivectomy ie gingival overgrowth
  • gingival graft
  • furcationplasty (re-shaping)
  • tunnel prep
  • flap surgery (perio flap surgery - gingival attachment to root - NEW JE ATTACHMENT)
  • guided tissue regeneration - most commonly used as it can ‘put back what has been lost’
179
Q

What are the different types of acute perio diseases

A
  • inflammation - chronic and acute
  • NG - acute perio disease, grey pseudomembrane
  • perio abscess/lateral perio abscess
  • pericorinitis
  • primary herpatic stomatitis

FINALS EXAM FLASHCARDS (5 decks)

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