The document discusses various controversies in periodontics, including classification, diagnosis, and treatment approaches for periodontal diseases. Key topics include the effectiveness of different therapies, the reliability of diagnostic methods, and the implications of systemic conditions on prognosis. The document highlights the complexity of periodontal disease management and the need for further research and consensus in the field.

1. CONTROVERSIES
IN
PERIODONTICS
DR. MANISHA SINHA
III YEAR PG
DEPT OF PERIODONTOLOGY
1RAJARAJESWARI DENTAL COLLEGE AND HOSPITAL

2.  CLASSIFICATION OF PERIODONTAL
DISEASES
 DIAGNOSIS OF PERIODONTAL
DISEASES
 PROGNOSIS
 TOOTH MOBILITY & SPLINTING
 GINGIVAL CURETTAGE ONE STAGE
FULL-MOUTH DISINFECTION VERSUS
QUADRANT SRP
 SYSTEMIC ANTIMICROBIALS IN
PERIODONTAL THERAPY
 NON-SURGICAL VERSUS SURGICAL
PERIODONTAL THERAPY
 POSTSURGICAL ANTIMICROBIAL MEDICATION
 PERIODONTAL PACK
 PERIODONTAL-ENDODONTIC RELATIONSHIP
 PERIODONTAL AND SYSTEMIC DISEASES
 IMPLANT THERAPY IN PERIODONTALLY
COMPROMISED PATIENTS
 CONCLUSION
 REFERENCES
2

3. INTRODUCTION
3

4. Lack of complete
knowledge and
understanding
Over dependence on
historical data
Lack of well
controlled, high
standard clinical
4

5. Controversies
5

6. 1. Which classification system best suits us?
2. Are the systems available reproducible?
3. Are all these systems based mainly on clinicians experience?
1.
6

7. The
Classical
pathology
paradigm
The
Infection/host
response
paradigm
Clinical
characteri
stics
paradigm
1970
1920-1970
7

8. 8

9. o How can the rate of progression be
estimated in a single visit?
o How do all the risk factors be
correlated with the amount of
destruction?
o With conventional diagnostic
techniques in everyday practice how
can the microbial & immunologic
status established?
• With the improved knowledge classification
systems have tried to be more
comprehensive.
• With the present chair side diagnostic
methods available it is impossible to
accurately determine the rate of destruction
,role of specific microorganisms &
immunologic background.
• A certain degree of overlap, confusion is
inevitable in border line cases.
9

10. How good are the conventional diagnostic methods?
Are the indices employed useful in clinical practice?
Can the etiological factors established consistently?
2.
10

11. The current diagnostic methods does rely too
much on historical/past events.
The current conventional diagnostic methods
despite several drawbacks are still relevant.
With the current diagnostic methods
factors cannot always be established
In many situations such as trauma from
occlusion, environmental risk factors, the
effect can not be established accurately.
11

12. With the current understanding of
disease process, can periodontal
disease prognosis be determined
accurately?
Do we have an evidence based
model to determine
prognosis?
Should prognosis be
determined in initial
examination?
3.
12

13. The complexity of
periodontal pathology
and the incomplete
understanding of the
same precludes the
clinician in
determining the
prognosis accurately.
Few systematic reviews &
meta analysis lead us to
believe that prognosis
prediction is accurate only
when the extremities are
considered viz very good, or
hopeless
At present we do not have
an evidence based model to
assist in the determination
of prognosis.
13

14. Prognosis of the
entire dentition
is not equivalent
to the sum total
of the prognosis
of individual
teeth.
Current evidence
does not
provide a basis
for assigning
prognostic
categories on
the basis of race.
Not enough is
known whether
there is any
difference in the
prognosis
between males
and females.
Except Diabetes
Mellitus and
HIV/AIDS, there
is not enough
evidence to
relate systemic
conditions with
periodontal
prognosis.
No conclusive
evidence to
show that
prognosis is
poor in
stressed
individuals
14

15. • Conflicting data
reported in various
studies precludes
the clinician in
making an accurate
determination of
prognosis except in
well-defined cases.
• Prognosis
determinatio
n should not
be rigid &
should be
reviewed
following
successive
stages of
treatment.
15

16. 4.
16

17.  SRP alone produces results that are clinically equivalent
to curettage + SRP
17

18. Does tooth
mobility
indicate poor
prognosis?
Are mobile
teeth more
prone for
periodontal
breakdown?
Should all
mobile
teeth be
splinted?Is the
therapeutic
outcome
different
between
mobile & non
5.
18

19. 19
• 1 • 2 • 3
Possibility of
bone repair in
presence of
active mobility if
infection &
inflammation are
controlled .
(Polson et al.
1983)
Increased
bone loss
over a
period of 10
years
(Nieri et al.
2002)
4
Poorer healing
response after
periodontal Rx
compared to
firm teeth
(Fleszar et al.
1980)
Less favorable
results after
regenerative
surgical therapy
(Cortellini et al.
2001)

20. Rosling et al. 1976
Same degree of bone fill in infrabony defects
adjacent to mobile & firm teeth
Klinge et al. 1985
No difference in healing between splinted &
mobile teeth following Rx of furcation defects by
GTR
20

21. o Non progressive tooth mobility does not always indicate poor prognosis.
o Better to have firm teeth while planning regenerative procedures.
o Provisional splinting.. to facilitate instrumentation.
21

22.  Is full mouth disinfection significantly superior to
the standard quadrant SRP?
CONTROVERSIES
6.
22

23. Advantages of full mouth disinfection
 More efficient use of treatment time
 Reduced number of treatment visits
 Reduced cost of therapy
 Improved clinical and microbiological results
23

24. CLINICAL OUTCOMES
 When FMDT was compared to quadrant SRP, the largest PD
reductions and gains in CAL occurred at ≥ 7 mm deep pockets
(Quirynen et al. 1995
Vandekerckhove et al. 1996
Mongardini et al. 1999
24

25. Reasons for conflicting results from studies
Effectiveness
of SRP
Point when measurements were assessed
( (i.e., before or after root planing)
Severity of disease in study
populations
25

26.  Lack of convincing evidence to support that FMDT approach
superior to traditional quadrant-wise therapy.
 Less time-consuming, yet equally efficacious clinically as the
standard quadrant SRP.
(Koshy et al. 2005, Wennstrom et al. 2005)
 Determine time availability, clinical workload & patient preference
while selecting Rx modality.
26

27.  Are the results of non surgical & surgical approaches
comparable?
 Are the results obtained following surgery maintainable?
 Does surgery actually prolong the life of the dentition?
7.
27

28. Effects of non surgical therapy-
o SRP - - reduce the amount of bacterial plaque & calculus attached to subgingival root
surface
o Total elimination of all bacteria & calculus from subgingival tooth surface is not possible
with any instrumentation techniques
o (Anderson et al. 1996
o Caffesse et al. 1986
Yukna et al. 1997)
28

29. PPD % of root surface still
covered with remnants
of plaque or calculus
after instrumentation
≤ 3 mm 4 - 43%
4–6 mm 15 - 38%
> 6 mm 19 - 66%
29

30. PPD Results
≤ 3 mm OFD results in more CAL loss than SRP
4–6 mm OFD results in less CAL gain than SRP
> 6 mm OFD results in more CAL gain than SRP
POSITION
The selection of surgical or nonsurgical periodontal therapy
should be based on a careful consideration.
30

31. Controversies
Should local drug
delivery agents be
used alone or as
an adjunct to
scaling and root
planing?
Are they substantially
effective in
improvement of
clinical outcomes?
8.
31

32. 32

33. 33

34. Position
The existing data appear insufficient to conclude that adjunctive sustained or
controlled release LDA treatment can either reduce the need for surgery or improve
long-term tooth retention, or is cost effective.
Additional studies are needed to support the use of LDAs in special sites
34

35. o Root surface biomodification.
o Reconstructive procedures Vs. OFD alone
o Effective reconstructive procedure(s) for
treating periodontal intraosseous defects
o Histologically evidenced regeneration or
mere bone fill
o Patient-centered outcomes.
9.
35

36. Favor Root Surface Biomodification
o New connective tissue attachment following citric
acid demineralization in animals (Polson & Proye
1983, Crigger et al. 1978, Klinge et al. 1981)
o New connective tissue attachment & some
regeneration following citric acid demineralization
in humans(Albair et al. 1982; Kersten et al. 1992)
36

37. Do not Favor Root Surface Biomodification
o No improvement in clinical outcomes when citric acid used in conjunction with
surgical procedures ± osseous grafts or GTR (Handelsman et al. 1991, Moore et
al. 1987, Renvert et al. 1985)
o No clinical improvements following use of EDTA root conditioning (Blomlof et
al. 1996, 1997)
o Meta-analysis on Root Surface Biomodification
Use of citric acid, tetracycline, or EDTA to modify the root surface provides no
benefit of clinical significance to regeneration in patients with chronic periodontitis
(Mariotti 2003)
37

38. GTR
o No significant difference in CAL gain & PD reduction between bioabsorbable & non
resorbable membranes
o GTR = GTR + bone grafts in treating infrabony defects. (Murphy & Gunsolley 2003)
o Additional usage of bone graft in a well-contained infrabony defect during GTR
treatment may be unnecessary (Murphy & Gunsolley 2003)
o No available data on either long-term clinical outcomes or patient-centered
outcomes
38

39. New CT
attachme
nt
Long junctional
epithelium
Nabers
&
O’Leary
1965
Haggert
y &
Maeda
1971
Listgarten &
Rosenberg 1979
Moskow et al.
1979
Autogenous Bone grafts
o Bone fill of 1.2 mm in defects treated
with autogenous intraoral grafts and
greater CAL gain compared with OFD
(Renvert et al. 1985)
o Significantly greater CAL gain & bone
fill compared to OFD alone (Reynolds
et al. 2003)
Histologic evaluations
39

40. Bone Fill
(mm)
Authors
FDBA 1.3 to 2.6 Altiere et al. 1979
Blumenthal & Steinberg 1990
DFDBA 1.7 to 2.9 Mellonig 1984
Quintero et al. 1982
Allografts
Allografts are superior to OFD in terms of bone fill (Reynolds et al.
2003)
40

41. Alloplasts
 Similar clinical results when compared to allografts (Barnett et al. 1989,
et al. 1989)
 Limited regenerative potential & no signs of new cementum or PDL
formation. (Nevins et al. 2000)
Xenografts
 Very little human clinical data to support use of xenografts for managing
periodontal defects (Mellonig 2000, Richardson et al. 1999)
41

42. New CT
attachment
No new CT attachment
Craig et
al. 2004
Parashis
et al.
2004
Parodi et al. 2000
Enamel Matrix Derivatives
o Inconsistent histologic evidence of regeneration
o Significant improvements in PD reductions &
radiographic bone fill than OFD alone (Scheyer
et al. 2002 Cardaropoli & Leonhardt 2002)
42

43. Root surface Biomodification
o Conflicting data in literature
o Favorable results not reproducible in humans
o Clinical value of this approach - - questionable
o No adverse effects of such treatment
GTR
o Superior to OFD in terms of CAL gain; PD reduction and
defect fill in treatment of deep infrabony defects
o GTR = GTR + Bone graft
43

44. Autografts & allografts
o Result in substantial bone fill
o Adequate clinical and histologic evidence of bone fill and periodontal
regeneration
o Recommended for treatment of infrabony defects
Alloplasts & xenografts
o Primarily function as biocompatible space fillers
o Produce clinical results similar to other bone replacement grafts or GTR
procedures
o Little or no regeneration of periodontal tissues 44

45. Combination of GTR and Grafts
o The combination of barrier membranes and grafting materials may result in
histological evidence of periodontal regeneration, predominantly bone repair.
o No additional benefits of combination treatments were detected in models of
wall infrabony, class 2 furcation or fenestration defects.
o In supra-alveolar and two wall infrabony (missing buccal wall) defect models of
periodontal regeneration the additional use of a grafting material gave superior
histological results of bone repair to barrier membranes alone { Sculean et al
EWP 2008 }
45

46. PERIODONTAL PLASTIC SURGERY
10
.
Controversies
o Is minimum zone of attached gingiva
mandatory?
o If found narrow, should the width of the
attached gingiva augmented necessarily?
o When orthodontic treatment is planned
should the augmentation be done prior to
or later?
o How predictable and sustainable are the
root coverage procedures?
Facts
o Inadequate” attached gingiva +
shallow vestibule favor subgingival
plaque accumulation & hinder oral
hygiene procedures (Friedman 1962,
Carranza & Carraro 1970, Corn 1962,
Rosenberg 1960)
o Thick marginal tissue prevent apical
progression of plaque-associated
periodontal lesions (Goldman 1951,
Ruben 1979)
o No requirement for a certain minimal
width of gingiva to maintain
periodontal health
46

47. o Even a narrow band of gingiva can withstand stress caused by
orthodontic forces (Coatoam et al. 1981)
o Significant gingival recession was observed after labial tooth movement
in monkeys (Batenhorst et al. 1974, Steiner et al. 1981)
o Difficulty to maintain proper plaque control due to presence of
appliances.
o If traumatic tooth brushing & plaque accumulation are etiological
factors, augmentation of keratinized gingiva is needed prior to 47

48. POSITION
o No need for augmentation of narrow attached
gingiva in patients practising optimal oral hygiene.
o Gingival augmentation is indicated for teeth selected
as abutments, requiring orthodontic corrections & at
implant sites.
o It is advisable to carry out gingival augmentation
prior to orthodontic treatment
48

49. o SCTG & CAF with or without GTR  most predictable
procedures for root coverage at present
o The use of Connective Tissue Graft or EMD with a
coronally advanced flap procedure enhances the
probability to obtain complete root coverage.
o Connective tissue graft with a coronally advanced flap
shows greater keratinized tissue gain over coronally
advanced flap alone.
o Barrier membranes do not improve the clinical benefits of
coronally advanced flap in terms of complete root
coverage
o (Cairo et al EWP 2008)
49

50. Is it justifiable to
remove supporting
bone?
Is positive bone
architecture
important?
In the light of current
knowledge of
Periodontal
pathogenesis, is pocket
eradication mandatory?
11.
50

51. o The reducing probing depths, CAL,
margin locations & gingival contour
obtained in the immediate post healing
phase are not sustainable over time.
o If plaque control is attained & other
patient risk factors are controlled,
positive bone architecture is not
mandatory to maintain health.
o Pocket eradication is not very vital
provided standard SPT is available.
o Resective osseous surgery has limited
use in advance cases, intra-bony defects.
o However, the results after ROS are more
predictable.
While the short term results
after ROS are good the
procedure has limited
indication since the emphasis
currently is regeneration and
conservation of tissues.
51

52. LASERS IN PERIODONTAL THERAPY
• Is there greater
clinical effect of laser
application
compared with
mechanical
debridement in
nonsurgical
periodontal therapy
in patients with
chronic
periodontitis?
• Is the use of lasers
safe in routine
clinical practice?
12.
52

53. o GaAlA diode laser  After 3
months of healing,
adjunctive laser treatment
resulted in a significantly
higher reduction in tooth
mobility, PD, and CAL.{
Kreisler et al 2005 }
o In particular, it was observed
that Er:YAG laser
monotherapy resulted in
significant improvements of
all the clinical and
microbiological parameters
Position
o Er:YAG laser application in
nonsurgical periodontal therapy
compared with mechanical
debridement resulted in similar
clinical outcomes.
o There is little evidence to support the
clinical application of either CO2,
Nd:YAG, Nd:YAP, or different diode
laser wavelengths.
53

54. CONTROVERSIES
o Does periodontal disease cause
pulpal necrosis?
o Does periodontal therapy cause
pulpal changes?
o Do severely periodontally involved
teeth with normal vitality
response, still require RCT as a
prophylactic measure?
o What is the effect of pulpless teeth
on periodontal tissues?
o Do endodontically treated teeth
respond differently to periodontal
therapeutic procedures?
o Can periodontal regenerative
techniques be attempted on
endodontically treated teeth?
13
.
54

55. FACTS
Effects of periodontal
disease on dental pulp:
- Possible pathways for
extension of periodontal
disease from pocket to the
pulp:
o Patent dentinal tubules
o Lateral canals
o Apical foramen or
foramina
o Only 2 out of 100 periodontally involved
teeth demonstrated lateral canals located in
a pocket.
o (Kirkham 1975)
o No or very few inflammatory cells in pulps of
resected / amputed roots from severely
periodontally involved teeth.
(Tagger & Smukler 1977
Haskell et al. 1980
55

56. Effects of endodontically involved
teeth on periodontal health and
healing:
-Negative effects of pulpless teeth
o Similarity of microbial flora
in root canals & deep
periodontal pockets
(A series of retrospective
studies by Jansson, Ehnevid,
Lindskog & Blomlof 1995,
1993)
o Gutta percha may trigger
macrophages to activate a bone-
resorptive system.
(Sjogren et al. 1998
Pascon et al. 1991
Tavares et al. 1994
Ricucci & Langeland 1998)
o In periodontitis patients, teeth
with endodontic treatment had
more bone loss as compared
with untreated contralaterals
(Timmerman & Van der Weijden
2006)
56

57. SYSTEMIC ANTIMICROBIALS IN
PERIODONTAL THERAPY
Controversies
Which periodontal conditions require systemic antimicrobials?
How severe does the periodontal infection have to be in order
to justify the use of an antimicrobial agent?
Should they be given to all individuals? If not, then who should
receive these agents?
14
.
57

58. oAdditional benefit of adjunctive
antimicrobials over SRP alone in
terms of CAL gain & PD
reduction, particularly at initially
deep periodontal pockets
(Herrera et al. 2002)
oAntibiotic provided significantly
better CAL gain of 0.3–0.4 mm
at 6 months post-therapy than
the comparison groups not
receiving antibiotic. (Haffajee et
o Valuable in the treatment of aggressive
periodontitis in adolescents, especially
cases predominated by A. a. comitans
(Slots & Schonfeld 1991)
o Antibiotics immediately after mechanical
debridement has proved to be more
beneficial than 3 / 6 months after
mechanical therapy
(Kaner et al. 2006)
58

59. Position
• Systemic
antimicrobials
are indicated
in patients
who show
progressive
attachment
loss despite
mechanical
therapy
• Aggressive
periodontal
conditions
benefit from
this therapy
59

60. POST SURGICAL
ANTIMICROBIAL
MEDICATION
Controversies
o Should antimicrobials be prescribed regularly in every case after
periodontal surgery?
o If antimicrobials are prescribed, then which one/combination?
oDo regenerative procedures benefit by antimicrobial medication?
15
.
60

61. Facts
o Reduced PO complications when
antibiotics given before
periodontal surgery & continued
for 4 to 7 days after surgery
(Ariaudo 1969;
Dal Pra & Strahan 1972;
Pendrill & Reddy 1980
o PO infection rates following
periodontal surgery without
antibiotics –
1 - 4.4% for routine periodontal
surgery
4.5% following implant surgery
(Gynther et al. 1998; Pack & Haber
1983;
Checchi et al. 1992)
61

62. oNot mandatory to prescribe antimicrobials in an
otherwise normal patient if proper aseptic &
infection control procedures have been followed
oLiterature data – Routine use of PO antibiotic
medication, whether indicated or not.
62

63. TO PACK OR NOT TO PACK :
THE CURRENT STATUS OF
PERIODONTAL DRESSINGS
Controversies
o Is it mandatory to use
periodontal dressings after
periodontal surgery?
o Which type of periodontal
dressings is most
commonly recommended?
o Are there any adverse
effects to use of
periodontal dressings?
o Are periodontal dressings
plaque retentive?
16
.
63

64. Clinical trials
in favour of
packing :
Ariaudo and Tyrell
et al
• Protection of wound from
mechanical trauma,
stability of the surgical site
during healing process
Prichard et al
• Patient comfort during
healing, good adaptation
to underlying gingival and
bony tissue, prevention of
postoperative
haemorrhage or
infection, decreasing tooth
64

65. 65

66.  Not mandatory to pack surgical sites in all
 Complete healing can take place even without a
dressing, provided the surgical area is kept clean
 There is no difference in healing between
dressed and nondressed wounds
 The choice of use of a periodontal dressing is a
matter of individual preference and the
judgment of the operator.
66

67. CVD STROKE
ADVERSE
PREGNANCY
OUTCOME
DIABETES
MELLITUS
Does the Evidence Support an
Independent Association?
17.
67

68. Aldridge etal, 1995 No effect on change in HbA1c
Christgau etal, 1998 No effect on HbAtc
Grossi etal, 1996, 1997 Significant reproductions (P≤ .04) in
mean HbA1c at 3 months
Iwamoto etal, 2001 A significant Improvement of HbA1c
levels: reduction inTNF- 𝛼 levels;
decreased Fasting insulin levels and
HOMA-R in patients not receiving Insulin
68

69. Offenbacher et al. 2001 Moderate-severe periodontal
(PR = 1.6) and progressive disease
(PR = 2.4) are significant risk
for preterm delivery
Jeffcoat et al. 2001 Severe or generalized periodontal
disease is associated with preterm
delivery (OR – 4.5)
Lopez et al. 2002b Significant association between
periodontal disease and preterm LBW
(RR = 3.5)
Boggess et al. 2003 Significantly higher risk for pre-
eclampsia among women with severe
(OR = 2.4) or progressive (OR = 2.1)
periodontal disease
69

70. IMPLANT THERAPY IN PERIODONTALLY COMPROMISED
PATIENTS
Does a history of periodontitis have an effect on
the long-term prognosis of implants?
Immediate vs. delayed implants ??
Implants in systemic conditions ??
18.
70

71.  Implants placed in partially edentulous
patients are more at risk for colonization
with periopathogens emerging from
periodontal pockets .
 Significantly higher bone loss after insertion of
the final abutment in GAP patients as
compared to CP patients over 3 years.
71

72.  Karoussis et al. 2003
Incidence of peri-implantitis
Periodontitis patients - - - 28.6% ;
Healthy patients - - - 5.8%
 Hardt et al. 2002
Mean peri-implant bone loss of >2 mm
64% of periodontitis patients ; 24%
of healthy patients
 Clinical success rate
Periodontitis patients - - - 52.4% ; Healthy
patients - - - 79.1%
 Survival rate
Periodontitis patients - - - 90.5%; Healthy
patients - - - 96.5%
(Karoussis et al. 2003)
72

73.  No statistically significant difference in the survival rates of implants in
individuals with periodontitis-associated and non periodontitis -associated
tooth loss over a period of 5 and 10 years. (Schou et al. 2006)
 In diabetes mellitus –
Dubey RK et al. 2013 – 85.5 – 100% (good / fair metabolic control)
Ferriera SD et al 2006 – increased risk of peri implantitis
Tawil G et al. 2008 – 45 patients – 9.1% ; overall – 3.9% failure rate
Oates et al. 2013 – limited evidence on impact of poor metabolic control on
implant
 Donos et al. – no evidence exists that states HIV as a contraindication for
implants 73

74. • No
contraindications
for implant
treatment in
periodontitis-
susceptible patients
Higher incidence of
peri-implantitis may
jeopardize longevity
of implant treatment
High survival rates for implants
in individuals with no H/o
periodontitis-associated tooth
loss
74

75. RECENT CONTROVERSY
• A/C researcher Shervin Molayem, DDS, a dental surgeon based on Los Angeles and
founder of the UCLA Dental Research Journal, the study suggests that COVID-19
patients with bad gums face a much greater risk of generating harmful IL-6 proteins that
spread to their lungs and trigger a life-threatening respiratory crisis.
• Plausible hypotheses supporting a potential bi-lateral link between periodontal diseases
and COVID-19 are encouraged to be tested.
75

76. CONCLUSION
76

77.  Armitage GC. Classifying periodontal diseases - a long-standing
dilemma. Periodontology 2000 2002; 30: 9-23.
 The American Academy of Periodontology statement regarding
gingival curettage. J Periodontol 2002; 73: 1229-1230.
 Haffajee AD. Systemic antibiotics: to use or not to use in the
treatment of periodontal infections. That is the question. J Clin
Periodontol 2006; 33: 359-361
 Seymour RA, Preshaw PM, Thomason JM, Ellis JS, Steele JG:
Cardiovascular diseases and periodontology. J Clin Periodontol
2003; 30: 279-292.
 Greenstein G. Full mouth therapy versus individual quadrant root
planing: a critical commentary. J Periodontol 2002; 73: 797-812
 Apatzidou DA. One stage full-mouth disinfection-treatment of
choice? J Clin Periodontol 2006; 33: 942-943. 77

78. 78