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BDS3: Clinical dental sciences > Periodontology > Flashcards

Flashcards in Periodontology Deck (113)
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1
Q

how is the 2017 disease classification graded?

A

1 - health
2 - plaque induced gingivitis (localised/ generlised)
3 - non plauqe induced gingival diseases nd conditions
4 - periodontitis
- periodontitis***
- localised (<= 30 teeth)
- molar incisor pattern>
5- necrotising perio diseases
6 - perio as a manifestation of systemic
7 - systemic disease or conditions affecting the periodontal tissues
8 - perio bscesses
9- perio-endo lesions
10- micogongival deformities and conditons

2
Q

how is clinical gingival health characterised?

A

absence of bleeding on probing, erythema and edema, patient symptoms, and attachment and bone loss

3
Q

what are the physiological bone levels range for clinical gingival health?

A

1.0 to 3.0 mm apical to the cemento-enamel junction

4
Q

how is gingival health defined?

A

For an intact periodontium and a reduced and stable periodontium, gingival health is defined as < 10% bleeding sites with probing depths ≤3 mm

5
Q

what is plaque induced gingivitis - intact periodontium?

A

BPEs 2 and no radiological bone loss and no interdental recession

6
Q

what is bleeding on probing in relation to localised or generalised?

A

<30% - localised
>30% - generalised

7
Q

what differentiates health and gingivitis

A

health <10% BOP
gingivitis >10% BOP

8
Q

what are plaque induced gingivitis modifying factors?

A

A. associated with bacterial dental biofilm only
B. potential modifying factors of plaque induced gingivitis
1. systemic conditions
a) sex steroid hormones
1) puberty
2) Menstrual cycle
3) pregnancy
4) oral contraceptive
b) hyperglcemia
c) leukemia
d) smoking
e) malnutrition
2. oral factors enhancing plaque accumulation
a) prominent subgigival restoration margins
b) hyposalivation
C. drug-influenced gingival enlargements

9
Q

what is plaque induced gingivitis - modified by puberty?

A

can be BPE 3s
no radiological bone loss
no interdental recession

10
Q

types of plaque induced gingivitis?

A

modified by puberty
modified by poor restorative margins
drug influenced gingival enlargement

11
Q

what are non plaque induced gingival diseases?

A
  • Genetic/developmental e.g. hereditary gingival fibromatosis
  • Specific infections e.g. herpetic gingival stomatitis, Candida albicans
  • Inflammatory/immune conditions – e.g. lichen planus
  • Inflammatory/immune conditions e.g. benign mucous membrane pemphigoid
  • Nutritional deficiency e.g. vitamin C deficiency
12
Q

what may occur in severely immune compromised nercotising periodontitis patients?

A

bone sequestrum

13
Q

what are necrotising perio diseases?

A
  • necrotising gingivitis
  • necrotising periodontitis
14
Q

what is a type of rare diseases that affect the course of periodontitis resulting in the early presentation of severe periodontitis.?

A

o Papillon Lefevre Syndrome
o leucocyte adhesion deficiency
o hypophosphatasia
o Down’s syndrome
o Ehlers-Danlos

15
Q

what are Systemic Diseases or Conditions Affecting the Periodontal Tissues?

A

Mainly rare conditions affecting the periodontal supporting tissues independently of dental plaque biofilm‐induced inflammation. This is a more heterogeneous group of conditions which result in breakdown of periodontal tissues and some of which may mimic the clinical presentation of periodontitis

16
Q

what are a more heterogeneous group of conditions which result in breakdown of periodontal tissues and some of which may mimic the clinical presentation of periodontitis.

A

o squamous cell carcinoma
o Langerhans cell histiocytosis

17
Q

what is recession type 1 for gingival recession?

A
  • Gingival recession with no loss of inter‐ proximal attachment.
  • Interproximal CEJ is clinically not detect‐ able at both mesial and distal aspects of the tooth.
18
Q

what is recession type 2 for gingival recession?

A
  • Gingival recession associated with loss of interproximal attachment.
  • The amount of interproximal attach‐ ment loss (measured from the interproximal CEJ to the depth of the interproximal sulcus/pocket) is less than or equal to the buccal attachment loss (measured from the buccal CEJ to the apical end of the buccal sulcus/pocket).
19
Q

what is recession type 3 for gingival recession?

A
  • Gingival recession associated with loss of interproximal attachment.
  • The amount of interproximal attach‐ ment loss (measured from the interproximal CEJ to the apical end of the sulcus/pocket) is greater than the buccal attachment loss (measured from the buccal CEJ to the apical end of the buccal sulcus/pocket)
20
Q

what is step 1 for the BSP treatment of perio diseases?

A

building foundations for optimal treatment outcomes
I: explain disease, risk factors and tx alternatives, risk and benefits including no treatment
II: explain importance of OHI, encourage and support behaviour change for OH improvement
III: reduce risk factors including plaque retentive features , smoking cessation and diabetes control interventions
IV: provide individually tailored OH advice including interdental cleaning. +/- adjunctive efficacious toothpaste and mouthwash, +/- professional mechanical plaque removal (PMPR) including supra and subgingival scaling of clinical crown
V: select recall period following published guidance and considering risk factors such as smoking diabetes
VI: oral health educator (I,II), hygienist therapist (I-IV), dentist, practitioner accredited for level 2 and 3 care (I-V)

21
Q

what do you do after step 1 for bsp guidelines of perio?

A

re-evaluate
non engaging patient repeat step 1
engaging patient move to step 2
consider referral

22
Q

what is step 2 of bsp guidelines for perio?

A

subgingival instrumentation (root surface debridement/ PMPR on root)
I: reinforce OH, risk factor control, behaviour change
II: subgingival instrumentation, hand or powered (sonic/ ultrasonic) either alone or in combination
III: use of adjunctive systemic antimicrobials determined by practitioner accredited for level 2 and 3 care

23
Q

what do you do after step 2 of bsp perio guidelines?

A

re-evaluate after 3 months
unstable -> step 3
stable -> step 4

24
Q

if step unstable and you go to step 3 for bsp perio guidelines what do you do?

A

managing non-repsonding sites:
I: reinforce OH, risk factor control, behaviour chnage
II: moderate (4-5mm) residual pockets - re-preform subgingival instrumentation
III: deep residual pocketing (6>=mm) consider alternative causes
IV: consider referral for pocket management or regenerative surgery
V: if referral not possible, re-perform subgingival instrumentation (if all sites stable after step 3 proceed to step 40

25
Q

if stable and you to step 4. what step 4 for the bsp perio guidelines?

A

maintenance
I: supportive periodontal care strongly recommended
II: Reinforce OH, risk factor control, behaviour change
III: regular targeted PMPR as required to loimit tooth loss
IV: consider evidence based adjunctive efficacious tooth paste and or mouthwash to control gingival inflammation

26
Q

after step 4 of bsp perio guidelines?

A

maintenance recall individually tailored intervals from 3 -12 months

27
Q

how do you define if a pt is engaging?

A

engaging - plaque levels <= 20 percent and bleeding levels <30 percent or 50 percent improvement

28
Q

what to do for decision making at re-evaluation? If he has Poor OH, persistent inflammation

A

 identify reason for poor OH, then supportive care or repeat cause-related therapy

29
Q

what to do for decision making for this perio lecture? Good OH, inflammation resolved?

A

 supportive care & proceed with treatment plan

30
Q

what to do for decision making for this perio lecture? Good OH, persistent deep pockets with BOP?

A

 consider surgical access or repeat RSD, then re-evaluate

31
Q

what is the ideal endpoint?

A

 No pockets > 4mm
 No pockets = 4mm with BOP
 BOP < 10%
 Functional and comfortable dentition
 Plaque scores < 20% (or target for patient)

 But not all patients will reach these….but they can still maintain a functional dentition…

32
Q

why supportive peridontal care?

A

 Patients who are not maintained in a supervised recall program subsequent to active treatment show obvious signs of recurrent periodontitis (e.g., increased pocket depth, bone loss, or tooth loss).
 The more often patients present for recommended supportive periodontal treatment (SPT), the less likely they are to lose teeth.
 Treated patients who do not return for regular recall are at 5.6 times greater risk for tooth loss than compliant patients.
 Patients who are not maintained in a supervised recall program subsequent to active treatment show obvious signs of recurrent periodontitis (e.g., increased pocket depth, bone loss, or tooth loss).
 The more often patients present for recommended supportive periodontal treatment (SPT), the less likely they are to lose teeth.
 Treated patients who do not return for regular recall are at 5.6 times greater risk for tooth loss than compliant patients.

33
Q

how is supportive periodontal car done?

A

3 separate parts.
 Part I – exam
- MH changes
- oral pathologic examination oral hygiene status (plaque chart)-
- gingival changed
- pocket depth changes
- mobility changes
- occlusal changes
- dental caries
- restorative, prosthetic and implant status

 Part II – treatment
- oral hygiene reinforcement
- supra gingival scaling
- root surface debridement
- polishing

 Part III: report, cleanup and scheduling
- write report in chart
- discuss report with pt
- schedule next recall visit
- schedule further periodontal tx
- schedule or refer for restorative or prosthetic tx

34
Q

what is part 1 exam of the supportive periodontal care?

A
  • Similar to the initial evaluation of the patient
  • Updating medical history
  • Oral mucosa inspected for pathologic conditions
  • Evaluation of restorations, caries, prostheses, occlusion, tooth mobility, bleeding on probing, and periodontal and periimplant probing depths
  • Analysis of the current oral hygiene status of the patient is essential.
  • The dentist primarily looks for changes that have occurred since the last evaluation
35
Q

what is part II treatment of supportive periodontal care?

A
  • Required scaling and root surface debridement (supra and subgingival PMPR) are performed, (based on pocket chart/plaque chart).
  • Care must be taken not to instrument normal sites with shallow sulci (1 to 3 mm deep – that do NOT have any calculus) because studies have shown that repeated subgingival scaling in initially normal periodontal sites result in significant loss of attachment.
36
Q

causes for recurrence of perio disease?

A
  • Often can be traced to inadequate plaque control on the part of the patient or failure to comply with recommended SPT schedules.
  • Inadequate or insufficient treatment that has failed to remove all the potential factors favoring plaque accumulation.
  • Incomplete calculus removal in areas of difficult access.
  • Inadequate restorations placed after the periodontal treatment was completed.
  • Failure of the patient to return for periodic checkups. This may be a result of the patient’s conscious or unconscious decision not to continue treatment or the failure of the dentist and staff to emphasize the need for periodic examinations.
  • Presence of some systemic diseases that may affect host resistance to previously acceptable levels of plaque.
37
Q

characteristics of necrotising periodontal diseases?

A

 The most severe inflammatory periodontal disorder caused by plaque bacteria
 Rapidly destructive and debilitating
 Due to shared predisposing factors in a population (e.g. students during a period of examinations, armed forces recruits) NPD are known to occur in epidemic-type patterns. This has led to the popular belief that NPD are contagious, but this is not the case.
 The main features of the NPD are painful, bleeding gums and ulceration and necrosis of the interdental papilla - punched-out appearance
 Opportunistic infection – caused by the bacteria inhabiting healthy oral cavity

38
Q

what are the classification of necrotising periodontal diseases?

A

necrotizing gingivitis
necrotizing periodontitis
necrotizing stomatitis

39
Q

what is necrotising ginigivits?

A

when only the gingival tissues are affected.

40
Q

what is necrotising periodontitis?

A

when the necrosis progresses into the periodontal ligament and the alveolar bone, leading to attachment loss.

41
Q

what is necrotising stomatitis?

A

when the necrosis progresses to deeper tissues beyond the mucogingival line, including the lip or cheek mucosa, the ton- gue, etc.

42
Q

what does foetor ex ore mean?

A

halitosis - bad breath

43
Q

what does halitosis mean?

A

bad breath

44
Q

what are the first lesions that are seen in necrotising gingivitis?

A

interproximally in mandiular anterior region

45
Q

what are necrotising periodonitis ulcers associated with?

A

deep pockets formation as gingival necrosis coincides with loss of crestal alveolar bone

46
Q

what happens with adenopathies?

A

submandibular lymph nodes are more affected than those in the cervical area

47
Q

what people have a greater severity of necrotising stomatitis lesions?

A

patients with severe systemic compromises pt - those with aids and pts with severe malnutrition

48
Q

what are some risk factors of necrotising periodontal diseases?

A

o In developed countries, NPD occurs mostly in young adults with predisposing factors such as psychological stress, sleep deprivation, poor oral hygiene, smoking, immunosuppression (HIV infection and leukaemia) and/or malnutrition.
o In developing countries, NPD occurs mostly in malnourished children.

49
Q

what are 2 main objectives of treatment of the acute phase for therapy?

A

1) to arrest the disease process and tissue destruction
2) to control the pt general feeling of discomfort and pain that is interfering with nutrition and oral hygiene practices

50
Q

what amtimicrobials could be used for tx of npd?

A

metronidazole 400mg TID 3 days

50
Q

what is treatment during the supportive or maintenance phase of treatment?

A

main goal is compliance with the oral hygiene practices and control of the predisposing factors

51
Q

what is necrotising periodontal disease suggestive of in systematically healthy individuals without any predisposing factors in background?

A

must be screened for HIV

52
Q

what is the treatment for the acute necrotising disease?

A
  1. ultrasonic debridement
  2. pain prevent patient from brush - instead 0.2 percent chlorohexidine mouth wash twice daily (previously 3% or 6% hydrogen peroxide)
  3. pts with malaise, fever and lassitude, lack of response to mechanical therapy and with impaired immunity
    200mg metronidazole TID (3 times daily) for 3 days
    400mg Metronidazole TID for 3 days
  4. smoking cessation, vitamin supplementation, dietary advice
  5. in case of necrotising periodontitis after remedy of acute symptoms you need to carry out hygiene phase therapy to treat perio disease
53
Q

what are some genetic conditions associated with the impairment of immune system in relation to periodontitis?

A

papillon-levre syndrome, chediak-higashi syndrome, LAS syndrome, down’s syndrome, chronic granulomatous disease

54
Q

what are some diseases leading to the impairment of immune system in relation to periodontitis?

A

leukaemia, agranulocytosis, neutropenia, HIV infection

55
Q

local acquired factors for periodontal diseases?

A

plaque, calculus, overhanging and poorly contoured restorations and prosthetic crowns, orthodontic appliances, occlusal trauma

56
Q

local anatomical factors for periodontal diseases?

A

malpositioned teeth, root groves, concavities and furcations, enamel pearls

57
Q

systemic non-modifiable risk factors for periodontal diseases?

A

aging, genetic factors, gender (males), genetic disorders: Down syndrome, Papillon-Lefevre syndrome.

58
Q

systemic modifiable risk factors for periodontal diseases?

A

smoking, poorly controlled diabetes, HIV, leukaemia, osteopenia, osteoporosis, stress, medications, hormonal status, poor nutrition, socioeconomic status

59
Q

why is smoking a risk factor to periodontal disease?

A

 Effect on oral microbiota
 Increase activation of the immune system
 Decreased healing capacity (reduced blood flow)

60
Q

why is sub-optimally controlled diabetes a risk factor to periodontal disease?

A

 Hyperglycaemia in diabetes may modulate
 RANKL ( the receptor activator of nuclear factor-kappa 𝛃): OPG (osteoprotegerin) ratio and thus contribute to alveolar bone destruction
 In hyperglycaemia production of AGE (advanced glycation end products) increases which leads to exacerbation of inflammation (production of pro-inflammatory cytokines and destructive metalloproteinases)

61
Q

what are important factors contributing to periodontal diseases severity for a patient with diabetes?

A
  • Degree of diabetic control
  • Age of onset
  • The duration of the disease
62
Q

why is obesity and nutrition a risk factor to periodontal disease?

A

 Severe vit. C deficiency – scorbutic gingivitis - scurvy
 Lack of nutrients - decrease function of the immune system

63
Q

why is drugs a risk factor to periodontal disease?

A

 Anticonvulsant: phenytoin
 Immunosupresants: cyclosporin (transplant patients)
 Calcium channel blockers (nifedipine,amlodipine)

64
Q

what does interaction between the drug and host fibroblasts result in, in regards to periodontal disease?

A

an increased deposition of connective tissue supporting a hyperproliferative epithelium>
e.g
- gingival enlargement hyperplasia - more fibroblasts
- gingival sweellign - more intercellular fluid increases permeabilisation of the vessels

65
Q

Why it is difficult to document cause-effect association between cardiovascular diseases and periodontitis?

A

o The same risk factors for both diseases (smoking, diabetes, stress, obesity)
o Common pathomechanisms associated with systemic inflammation and activation of the immune system

66
Q

what is periodontitis a risk factor for?

A
  • rheumatoid arthritis
  • preeclampsia
  • Alzheimer’s disease
67
Q

what are types of Abscesses of the Periodontium?

A

o Gingival abscess. Localised to gingival margin
o Periodontal abscess:
o Pericoronal abscess:
o Endodontic-Periodontal Lesion:

68
Q

what is periodontal abscess?

A
  • usually related to preexisting deep pocket also associated with food packing and tightening of gingival margin post HPT
  • Rapid destruction of periodontal tissues, with a negative effect on the prognosis of the affected tooth
69
Q

what is pericoronal abscess?

A

associated with partially erupted tooth most commonly 8s

70
Q

what is endodontic-periodontal lesion?

A
  • tooth is suffering from varying degrees of endodontic and periodontal disease
  • EPL is a pathological communication between the endodontic and periodontal tissues of a given tooth
71
Q

what are signs and symptoms of abscess?

A

o Swelling
o Pain
o Tooth may be TTP in lateral direction
o Deep periodontal pocket
o Bleeding
o Suppuration
o Enlarged regional lymphnodes
o Fever
o Tooth usually vital
o Commonly pre-existing periodontal disease

72
Q

what do the SDCEP guidelines tell you about how to treat abscess?

A

o Carry out careful sub-gingival instrumentation short of the base of the periodontal pocket to avoid iatrogenic damage; local anaesthesia may be required.
o If pus is present in a periodontal abscess, drain by incision or through the periodontal pocket.
o Recommend optimal analgesia.
o Do not prescribe antibiotics unless there are signs of spreading infection or systemic involvement.
o Recommend the use of 0.2% chlorhexidine mouthwash until the acute symptoms subside.
o Following acute management, review and carry out definitive periodontal instrumentation and arrange an appropriate recall interval.

73
Q

what do you do if puss is present in a periodontal abscess?

A

drain by incision or through the periodontal pocket.

74
Q

you do not prescribe antibiotics until there are signs of what in relation to an abscess?

A

Do not prescribe antibiotics unless there are signs of spreading infection or systemic involvement.

75
Q

what do you recommend the use of until the acute symptoms of an abscess subside?

A

Recommend the use of 0.2% chlorhexidine mouthwash until the acute symptoms subside.

76
Q

what are the systemic antiobiotics treatment you give for periodontal abscess?

A

 Only if signs of spread and systemic effects or if symptoms do not resolve with local measures
 Careful RSD
 Penicillin V 250mg(preferred) or Amoxicillin 500mg 5 days
 Or
 Metronidazole 400mg 5 days

77
Q

what are the 4 components of the peridoontium?

A
  • gum or gingiva
  • periodontal ligament
  • cementum
  • alveolar bone
78
Q

what is the PDL?

A

attachment fibres fastening tooth to the bone

79
Q

what is cementum?

A

covering and holding the root?

80
Q

what is alveolar bone?

A

where the root is anchored

81
Q

what is acute endo periodontal lesion”

A

o Trauma
o Perforation

82
Q

what is chronic endo periodontal lesion?

A

o Pre-existing periodontitis
o Slow and chronic progression without evident symptoms

83
Q

what are the signs and symptoms of an endo periodontal lesion?

A

o deep periodontal pockets reaching or close to the apex
o negative or altered response to pulp vitality tests
o bone resorption in the apical or furcation region
o spontaneous pain
o Pain on palpation and percussion
o Purulent exudate
o tooth mobility
o sinus tract
o crown, and gingival colour alterations

84
Q

what is main route of communication between pulp and periodontium?

A

apical foramen

85
Q

what is apical foramen role in communicating between pulp and periodontium?

A
  • Microbial and inflammatory by-products may exit the apical foramen causing periradicular pathoses.
  • The apex is a portal of entry for inflammatory by-products from deep periodontal pockets to affect the pulp.
86
Q

what does perforation result in?

A

Results in communication between the root-canal system and either peri-radicular tissues, periodontal ligament or the oral cavity.

87
Q

what are causes of perforation?

A

 extensive dental caries
 resorption
 operator error e.g. root-canal instrumentation or post preparation

88
Q

what are the Endo‐periodontal lesions associated with trauma and iatrogenic factors?

A

o root/pulp chamberfurcation perforation (e.g. because of root canal instrumentation or to tooth preparation for post‐retained restorations)
o root fracture or cracking (e.g., because of trauma or tooth preparation for post‐retained restorations)
o external root resorption (e.g., because of trauma)
o pulp necrosis (e.g., because of trauma) draining through the periodontium

89
Q

what is treatment of perio-endo lesions?

A

 Carry out endodontic treatment of the affected tooth.
 Recommend optimal analgesia.
 Do not prescribe antibiotics unless there are signs of spreading infection or systemic involvement.
 Recommend the use of 0.2% chlorhexidine mouthwash until the acute symptoms subside.
 Following acute management of the lesion, review within ten days and carry out supra- and sub-gingival instrumentation if necessary and arrange an appropriate recall interval

90
Q

Does endodontic disease affect periodontal health?

A

 When the pulp becomes infected, it elicits an inflammatory response in the periodontal ligament at the apical foramen and/or adjacent to openings of the small portals of exit

90
Q

endo infection in mandibular molars was associated with more attachment loss in what area?

A

furcal area

91
Q

how does endo infection in molars associated with periodontal disease enhance periodontitis progression?

A

by spreading pathogens through accessory canals and dentinal tubules

92
Q

Does periodontal disease affect endodontics

A

 no effect on the pulp, at least until it involves the apex
 Periodontal disease on the pulp is degenerative and causes calcification, fibrosis and collagen resorption, as well as a direct inflammatory affect

93
Q

Pulp is usually not significantly affected by periodontal disease until when?

A

until recession affects a lateral or accessory canal to the mouth.

94
Q

what is Function of the periodontium?

A

o To attach the teeth to the jaws
o To dissipate occlusal forces

95
Q

what is effective occlusal force?

A

occlusal force that exceeds the reparative capacity of the periodontal attachment apparatus, which results in occlusal trauma and/or causes excessive tooth wear (loss).

96
Q

what does occlusal trauma describe?

A

injury resulting in tissue changes within the attachment apparatus, including periodontal ligament, supporting alveolar bone and cementum, as a result of occlusal force(s).

97
Q

what could tooth mobility indicate?

A

May indicate successful adaptation of the periodontium to functional demands and/or reflect the nature of the remaining attachment

98
Q

Tooth mobility can be accepted, unless?

A

 It is progressively increasing
 It gives rise to symptoms
 It creates difficulty with restorative treatment

99
Q

what is therapy used to reduce tooth mobility?

A

o Control of plaque-induced inflammation.
o Correction of occlusal relations.
o Splinting.

100
Q

what is primary occlusal trauma?

A

Injury resulting in tissue changes from excessive occlusal forces applied to a tooth or teeth with normal periodontal support. It occurs in the presence of normal clinical attachment levels, normal bone levels, and excessive occlusal force(s).

101
Q

what is the response of the healthy periodontium?

A

o PDL width increases until forces can be adequately dissipated, the PDL width should then stabilise
o Tooth mobility will be increased as a result
o This can be regarded as successful adaptation to increased demand and therefore physiological
o If demand is subsequently reduced, PDL width should return to normal
o If the demand of occlusal forces is too great or the adaptive capacity of the PDL reduced, PDL width may continue to increase
o PDL width and tooth mobility fail to reach a stable phase
o This failure of adaptation may be regarded as pathological

102
Q

what is secondary occlusal trauma?

A

o injury resulting in tissue changes from normal or excessive occlusal forces applied to a tooth or teeth with reduced periodontal support.
o It occurs in the presence of attachment loss, bone loss, and normal/excessive occlusal force(s).

103
Q

what is fremitus?

A

o palpable or visible movement of a tooth when subjected to occlusal forces.

104
Q

what is tooth migration?

A

o Loss of periodontal attachment
o Unfavourable occlusal forces
o Unfavourable soft tissue profile

105
Q

what is management of tooth migration?

A

o Treat the periodontitis
o Correct occlusal relations
o Either:
 (a) Accept the position of the teeth and stabilise or
 (b) Move the teeth orthodontically and stabilise

106
Q

what is effect on periodontal therapy in relation to tooth mobility and occlusal forces?

A

o Decreased CAL gain post HPT.
o Increased Clincal Attatchment loss over time
o Mobile teeth treated with regeneration do not respond as well as non‐mobile teeth.
o But no association was drawn between mobility and occlusal forces.

107
Q

studies found that teeth with occlusal discrepancies had what?

A

o deeper initial probing depths
o more mobility
o poorer prognoses than those teeth without occlusal discrepancies.

108
Q

how to correct occlusal relations?

A

o Occlusal Adjustment (Selective Grinding)
o Restorations
o Orthodontics

109
Q

Splinting may be appropriate when?

A

o Mobility is due to advanced loss of attachment
o Mobility is causing discomfort or difficulty in chewing
o Teeth need to be stabilised for debridement.

110
Q

however what does splinting not influence?

A

o Does not influence the rate of periodontal destruction

111
Q

what may splinting create?

A

o May create hygiene difficulties
o Is a treatment of “last resort”