This document provides an overview of interdisciplinary periodontics, covering interactions between periodontics and other dental specialties. It discusses the relationship between periodontics and endodontics, orthodontics, prosthodontics and restorative dentistry, oral surgery, oral pathology, and oral and maxillofacial radiology. For each interaction, it describes clinical findings, diagnoses, treatments, and prognoses. The document focuses in depth on endodontic-periodontal interactions and the relationship between orthodontics and periodontics.

1. GOOD
MORNING!!
1

2. Interdisciplinary
periodontics

3. Contents
 Introduction
 Interaction between endodontics and periodontics.
 Effect of orthodontic treatment on the periodontal tissues
 The periodontal restorative interface: esthetic considerations
 Pedodontic-Periodontal interactions
 Maxillofacial Radiology & Periodontology
 Relationship with Oral Pathology
 Oral Surgery and Periodontology
 Conclusion
 References
3

4. INTRODUCTION
⩥ Periodontics is not practiced in isolation, as frequently
many patients have multiple dental needs or medical
health issues that require management.
⩥ In addition, pathology that manifests in the periodontal
tissues, and the onset and progression of periodontitis can
be affected by systemic conditions, such as diabetes, and
vice versa.
4

5. Interactions of Periodontology
5
Periodontology
Endodontics
Prosthodontics
& Restorative
Dentistry
Dental
Implantology
Orthodontics
Oral &
Maxillofacial
Radiology
Oral Surgery
Oral
Pathology
Geriatrics
General
Medicine

6. 1. Endodontic-
periodontal interactions
Most commonly encountered

7. ⩥ In 1964, Simring and Goldeberg - first described the
relationship between endodontics and periodontics.
⩥ ENDODONTIC LESION is used to denote an inflammatory
process in the periodontal tissues resulting from noxious
agents present in the root canal system of the tooth, usually a
root canal infection.
⩥ PERIODONTAL LESION is used to denote an inflammatory
process in the periodontal tissues resulting from accumulation
of dental plaque on the external tooth surfaces.
7

8. ⩥ Pulp & periodontium interrelation:
⩥ Turner & Drew (1919): 1st described effect of periodontal
disease on pulp.
⩥ Simring & Goldberg (1964): 1st described relationship
between periodontal & pulpal disease
8
Embryonic Anatomic Functional

9. Historic outlook
⩥ Cahn (1927) was one of the first investigator to state that
periodontal disease had an influence on the pulpal tissue. This
influence to the close proximity of these structures in the
region of the apical foramen.
⩥ Bender (1936), in a study reported that a large number of
extracted teeth had lateral and accessory canals. He
presented evidence that pulpal inflammation and degeneration
could result from periodontal disease.
⩥ Chacker (1974) in his studies, described vascular
anastomoses through lateral and accessory canals. He also
commented on the potential for communication through
exposed dentinal tubules.
9

10. ⩥ Torabinejad (1985) studied 25 teeth from a single patient
and could not establish any interrelationships between
periodontal and pulpal diseases.
⩥ Hiatt (1977) and Hemington (1979) stated that there is no
apparent relationship between periodontal and pulpal
disease.
10

11. CLASSIFICATION OF PULPAL DISEASES
11

12. CLASSIFICATION OF PERIRADICULAR
DISEASES
12

13. Etiology
LIVE PATHOGENS
⩥ Encountered in a diseased pulp and in periradicular tissues may include
bacteria, fungi and viruses.
1) BACTERIA
⩥ Play a crucial role in the formation and progression of both endodontic and
periodontal diseases .
⩥ The periradicular tissues become involved when bacteria invade the pulp,
causing either partial or total necrosis.
⩥ Kakehashi et al. 1965, in a classic study, demonstrated the relationship in their
study, pulps of normal rats were exposed and left open to the oral environment.
⩥ Consequently, pulp necrosis ensued, followed by inflammation of periradicular
tissue and lesion formation.
⩥ However, when the same procedure was performed on germ-free rats, not only
did the pulps remain vital and relatively noninflamed, the exposure sites showed
evidence of dentin repair.
13

14. ⩥ Similar studies were performed by various authors in different years
to confirm the finding;
(Moller et al1981, Blomlof et al 1992, Rupf et al 2000)
⩥ Specific PCR methods detected;
1. Aggregatibacter actinomycetemcomitans,
2. Tannerella forsythia,
3. Eikenella corrodens,
4. Fusobacterium nucleatum,
5. Porphyromonas gingivalis,
6. Prevotella intermedia and
7. Treponema denticola (spirochetes)
8. L-phase bacteria
⩥ These pathogens were found in all endodontic samples and also in
teeth with chronic apical periodontitis and chronic adult periodontitis. 14

15. 2) Fungi (Yeasts)
⩥ Presence and prevalence of fungi associated with endodontic disease
is well documented.
⩥ Fungal colonization associated with radicular pathosis has been
demonstrated in untreated root caries, dentinal tubules, failing root-
canal treatments , apices of teeth with asymptomatic apical
periodontitis and periradicular tissues.
⩥ Majority of the recovered fungi were candida albicans.
⩥ Fungi colonization :
1. Immune compromising diseases such ascancer
2. Certain intra canal mediaments,
3. Local and systemic antibiotics and
4. Previous unsuccessful endodontic therapy.
15

16. ⩥ Reduction in the numbers of specific strains of bacteria in the root
canal during endodontic treatment may allow fungal overgrowth in
the remaining low nutrient environment.
⩥ Another possibility is that fungi may gain access to the root canal
from the oral cavity as a result of poor asepsis during endodontic
treatment or post-preparation procedures.
⩥ In addition, it has been demonstrated that the presence of fungi in
root canals is directly associated with their presence in saliva and
oral tissues .
⩥ These findings further stress the importance of using aseptic
endodontic and periodontal techniques, maintaining the integrity of
dental hard tissues and covering the tooth crown as soon as practical
with a well-sealed permanent restoration in order to prevent
reinfection. 16

17. 3) Viruses
⩥ There is increasing evidence to suggest that viruses plays an
important role in both endo-perio disease.
⩥ Herpes simplex virus is frequently detected in Gingival
crevicular fluid and periodontal lesions.
⩥ Cytomegalovirus was found in about 55% of periodontal
pocket (Hutter 1991).
⩥ Epstein-Bair Virus type 1 was detected in more than 40% of
pocket (Slots et al 1988).
⩥ Sabet et al suggested that human cytomegalovirus and EB
virus play a role in the pathogenesis of symptomatic
periapical lesions. 17

18. Non-living etiologic agents
A. Extrinsic agents
1. Foreign Bodies
⩥ Dentin and cementum chips, amalgam, root canal
fillingmaterials, cellulose fibers from absorbent paper points,
gingival retraction cords, leguminous food and calculus like
deposits.
⩥ Response to foreign body – acute or chronic reaction –
symptomatic or asymptomatic conditions.
⩥ Mechanical or surgical removal of the foreign body is the
treatment of choice.
18

19. B. Intrinsic agents.
1. Cholesterol
⩥ Present in apical periodontitis ( Histopathologic finding) - induce a
typical foreign body reaction.
⩥ Cholesterol released by disintegrating erythrocytes of stagnant
blood vessels within periapical lesion lymphocytes, plasma cells
which die in great numbers and disintegrate in chronic periapical
lesions or by the circulating plasma lipids.
⩥ Accumulation of cholesterol crystals in inflamed periapical tissues
- causes of failure of Endo therapy
19

20. 2. Russell Bodies
⩥ Found in most inflamed tissues, accumulations of an
eosinophilic substance.
⩥ Caused by the synthesis of excessive amounts of normal
secretary protein in certain plasma cells engaged in active
synthesis of immunoglobulins.
3. Rushton hyaline bodies
⩥ Unique feature of some odontogenic cysts.
⩥ They are keratinous in nature, of hematogenous origin, a
specialized secretory product of odontogenic epithelium.
20

21. Biologic effects of pulpal Infection on periodontal tissues
21

22. Progression of the pulpal and periradicular
pathosis
22

23. Classification of endo-perio lesions
⩥ Based on etiology by Simon, Glick and Frank 1972
23
Type 1
Primary endodontic
lesions
Type 5
True combined lesions.
Type 4
Primary periodontal
lesions with secondary
endodontic
involvement.
Type 3
Primary periodontal
lesions
Type 2
Primary endodontic
lesions with secondary
periodontal
involvement.

24. 24

25. ⩥ Torabinejad and Trope classification (1996) - Based on the
origin of the periodontal pocket.
25
Endodontic origin
Lesions with no
communicstion
Lesions with
communication
Separate endodontic &
periodontal lesions
Combined endo-perio
lesion
Periodontic origin

26. AAP 1999 CLASSIFICATION
Periodontitis Associated with Endodontic
Disease
26
ENDODONTIC-
PERIODONTAL LESION
COMBINED LESION
PERIODONTAL-
ENDODONTIC LESION

27. Primary Endodontic lesions
Causes:
⩥ Deep caries.
⩥ Large restorations.
⩥ Traumatic injuries.
⩥ H/o pulp capping or pulpotomy.
⩥ Poor RCT.
Characteristics/C/F:
⩥ Tooth mobility.
⩥ Narrow pocket.
⩥ Swelling in mucobuccal fold.
⩥ Tenderness to percussion.
⩥ Severe pain
⩥ Sinus tract
⩥ Localized bone loss
27

28. Diagnosis:
⩥ Radiographs
⩥ Pulpal test:Negative.
⩥ Rapid onset.
⩥ Tracing of Sinus tract.
⩥ Periodontal probing.
Treatment:
⩥ Complete resolution- after
conventional endodontic therapy.
⩥ Prognosis- Excellent
28
Images: (A) Abscess on the buccal aspect of the tooth is traced
with a gutta-percha cone.
(B) Periapical radiograph showing radiolucency associated with
the mesial and distal roots, as well as the furcation area.
(C) Radiograph taken 4 months after root-canal therapy showing
active bony healing.
(D) Clinically, the buccal periodontal defect has healed and
probing is normal.

29. Primary Endodontic lesions with secondary
periodontal involvement
Causes:
⩥ Untreated primary endodontic lesion.
⩥ Plaque/calculus
⩥ Restoration of crown where pins and posts are
misplaced
⩥ Root perforation
Characteristics/C/F:
⩥ Long standing pulpal pathoses.
⩥ Superimposition of plaque/calculus.
⩥ Generalized periodontal disease.
Diagnosis:
⩥ Pulpal test: -ve.
⩥ Significant periodontal inflammation.
⩥ Radiographic evidence of angular defects
⩥ At the initial site of the endo involvement.
⩥ Periodontal probing
29

30. Treatment
⩥ Endodontic treatment
⩥ Periodontic treatment
⩥ With endodontic therapy only part of the lesion can be expected to
heal.
⩥ According to Ingle and Beveridge prognosis of primary periodontal
lesions is not as favorable as primary endodontic lesions.
⩥ It has been seen bone loss due to endodontic lesion is reversible but
irreversible due to periodontal lesion.
Prognosis
⩥ For endodontic lesion is superior
⩥ Periodontal therapy depends on the severity of periodontal
involvement.
⩥ Must receive regular maintenance
30

31. 31

32. Primary Periodontal lesions
Characteristics
⩥ Teeth vital
⩥ Generalized bone loss
⩥ Calculus/plaque
⩥ Soft tissue inflammation
⩥ Broad based pockets
⩥ Mobility
⩥ Periodontal abscess during acute phase
Diagnosis
⩥ Visual examination
⩥ Probing
⩥ Pulp testing- POSITIVE
⩥ Radiographs 32

33. Treatment
⩥ Periodontal therapy
⩥ Root amputation
⩥ Guided tissue regeneration
⩥ Root canal therapy(advance cases)
Prognosis
⩥ Depends on the outcome of periodontal therapy.
⩥ Depends on the extent of the periodontitis and on patients ability
to comply with potential long term treatment and maintenance
therapy.
33

34. Primary periodontal lesion with secondary endodontic
involvement.
Characteristics
⩥ Deep periodontal pockets > 6-8mm
⩥ History of extensive periodontal procedures
⩥ Irreversible pulpal pathosis
⩥ Large restorations
Symptoms
⩥ Sensitivity to temperature
⩥ Tenderness to purcussion
⩥ Mobility
⩥ Swelling
Diagnosis
⩥ History of disease progression
⩥ Probing
⩥ Pulp testing
⩥ Radiographic changes
34

35. Treatment
⩥ Periodontal therapy
⩥ Root amputation
⩥ Guided tissue regeneration
⩥ Root canal therapy
Prognosis
⩥ Depends on continuing periodontal treatment subsequent to
endodontic therapy.
35

36. 36

37. True combined lesions
⩥ It arises when an endodontic disease progressing coronally joins
with an infected periodontal pocket progressing apically.
Characteristics
⩥ Once the pulpal and periodontal lesions coalesce, they may be
clinically indistinguishable.
⩥ Necrotic pulp/ failed endodontic treatment, plaque, calculus and
periodontitis will be present in varying degrees.
Diagnosis
⩥ Probing
⩥ Radiographs
⩥ Pulpal testing: negative.
37

38. Treatment
⩥ Endodontic therapy
⩥ Periodontal therapy.
⩥ Hemisection
⩥ Bicuspidization
⩥ Root amputation
Prognosis
⩥ Depends on the each individual factor.
⩥ Adequate root canal therapy results in resolution of the
periapical lesion
⩥ Prognosis of the affected tooth then depends totally on the
outcome of periodontal therapy.
38

39. 39
True combined endodontic–periodontal
disease.
(A) Radiograph showing bone loss in two-
thirds
of the root
with calculus present and separate periapical
radiolucency.
(B) Clinical examination revealed coronal
color
change of the tooth involved and pus
exuding
from the
gingival crevis. Pulp-sensitivity tests were
negative.

40. 40
True combined endodonticperiodontal
diseases
(A) Preoperative radiograph showing
periradicular radiolucencies. Pulp sensitivity
tests were negative.
(B) Immediate postoperative radiograph of
nonsurgical endodontic treatment.
(C) Six-month follow-up radiograph showing
no healing. Gutta-percha cone is inserted in
the buccal gingival sulcus.
(D) Clinical photograph showing treatment
of the root surfaces and removal of the
periradicular lesion.
(E) One-year follow-up radiograph
demonstrating healing.

41. 2. Ortho-Perio
relationship

42. INTRODUCTION
⩥ A magnificent orthodontic treatment can be destroyed by
poor periodontal support.
⩥ Thus evaluation and maintenance of periodontal health
before , during and after treatment is very important.
⩥ Edward H. Angle (1899) for the first time advocated the
correlation between Orthodontics and Periodontics.
42

43. ⩥ OBJECTIVE:
To restore and maintain the health and integrity of the
attachment apparatus of teeth.
⩥ RISK ASSESSMENT BEFORE ORTHODONTIC
TREATMENT
1. Bleeding on probing
2. Tooth mobility
3. Thin fragile gingiva
4. Pockets
43

44. PERIODONTAL PROBLEMS DURING
ORTHODONTIC TREATMENT
⩥ Gingival hyperplasia can develop after 1-2 months
of orthodontic appliance being placed.
⩥ It may also interfere with completion of orthodontic
treatment
44

45. ⩥ SCALING:
Professional scaling indicated during active intrusion of
elongated maxillary incisors because orthodontic
intrusion may shift supragingival plaque to a sub-gingival
location. (Ericsson, 1977 & 1978; Melsen 1988 & 1992)
45

46. PROBLEMS AFTER ORTHODONTIC
TREATMENT
46
Black triangles
Open gingival embrasures “black triangles” are defined as the
embrasures cervical to the inter-proximal contact that is not filled by
gingival tissues.

47. ⩥ RELAPSE:
Transseptal fibres stretches elastically thus pulling the
tooth back to it’s original position.
⩥ Prevention:
1. Permanent retention - bonded retainers
2. Removable plates or spring retainers
47

48. ⩥ Tooth mobility: Due to excessive orthodontic
forces
⩥ Intrabony pockets
⩥ Inability to maintain oral hygiene
⩥ Gingivitis
⩥ Halitosis / breath malodour
48

49. EFFECTS OF ORTHODONTICS TREATMENTS ON
THE PERIODONTIUM
⩥ Short Term :
1. Gingivitis
2. Gingival Enlargement
3. No Attachment Loss
Effects : Reversible
⩥ Long Term :
1. Root Resorption
2. Attachment Loss
Effects : Irreversible
49

50. 50
RESPONSE OF THE ‘PDL’ TO
ORTHODONTIC FORCES
⩥ Slightly excessive pressure stimulates resorption of alveolar
bone, with compression of PDL fibres – Pressure zone.
⩥ Slightly excessive tension causes elongation of PDL fibers &
apposition of alveolar bone – Tension zone

51. 51

52. 52
⩥ Orthodontic forces within the adaptive capacity of
periodontium: Direct / frontal bone resorption

53. ⩥ Not within the adaptive capacity of periodontium:
Undermining / Indirect bone resorption
53
Hyalinization of tissues
Osteoclasts appear in
marrow spaces
Undermining Bone
Resorption
• Apposition of bone in
tension zone
• Temporary hypermobility
of tooth
• When the effects of
forces have nullified,
healing of pressure &
tension zones occur

54. ⩥ Injury to the periodontium produces a temporary
depression in mitotic activity and the rate of
proliferation of fibroblasts, collagen and bone
formation.
⩥ These return to normal levels after dissipation of the
forces.
54

55. RESPONSE OF BONE TO ORTHODONTIC
FORCES
⩥ Bone surrounding a tooth subjected to a force shows;
⩥ Resorption in areas of pressure pressure.
⩥ New Bone deposition in areas of tension.
55

56. COMPLICATIONS AFTER ORTHODONTIC
TREATMENTS
⩥ Mouth Breathing
⩥ Tongue Thrusting
⩥ Gingival Hyperplasia
⩥ Un-erupted teeth ankylosis
⩥ Gingival Recession
⩥ Tooth mobility
56

57. Treatment
CIRCUMFERENTIAL SUPRACRESTAL
FIBEROTOMY
⩥ The term “circumferential supracrestal fiberotomy” was
first introduced not only transect free gingival fibers but
also trans-septal ones.
-(Campbell etal 1975)
⩥ Supra-alveolar fibers do not adapt to new tooth positions
and are in part responsible for relapse.
-(Thompson etal)
57

58. ⩥ INDICATIONS
1. Rotated teeth
2. Crowded mandibular teeth.
3. Midline diastemas
⩥ CONTRAINDICATIONS
1. Poor oral hygiene, gingivitis or periodontal
pocketing.
2. Gingival recession or lack of attached
gingiva
58

59. PERIODONTAL ACCELERATED
OSTEOGENIC ORTHODONTICS
⩥ Periodontal accelerated osteogenic orthodontics
(PAOO) is a clinical procedure that combines :
1. Selective alveolar corticotomy,
2. Particulate bone grafting,
3. Application of orthodontic forces.
59

60. ⩥ RESULTS OF “PAOO”
1. An increase in alveolar bone width
2. Shorter treatment time
3. Increased post- treatment stability
4. Decreased amount of apical root resorption
60

61. ⩥ DISADVANTAGES OF “PAOO”
1. Additional cost.
2. Morbidity associated with surgery.
3. Post-operative pain.
4. More discomfort with arch wire activation.
5. Highly Skilled Periodontal procedure
61

62. 3. Periodontal-
restorative
relationships

63. RATIONALE FOR PERIODONTAL THERAPY
⩥ Stable gingival margins should be before tooth
preparation (Kois 2000)
⩥ Perio treatment should antecede restorative care.
⩥ Quality, quantity and topography of the periodontium
provides structural defense factors in maintaining
health.
63

64. NORMAL PERIODONTIUM
⩥ Gingiva
⩥ Gingival crevice
⩥ Biologic width
64

65. IRRITATING FACTORS FOR
PERIODONTIUM
Prior to procedure
⩥ Caries
⩥ Teeth separation
⩥ Rubber dam
During the procedure: meticulous instrumentation.
⩥ Preparation instrumentation
⩥ Vibration
⩥ preserving proximal plate of enamel-during gross cavity preparation-
avoid injury to gingiva.
⩥ Wedges below contact area- before proximal box preparation
⩥ Matricing
65
Interactions between the gingiva and the margin of restorations, J Clin Periodontol 2003; 30: 379–385.

66. Long after the procedure: restoration in close proximity to soft
tissue.
⩥ Gingival retraction
⩥ Physical retraction methods
⩥ Chemical retraction methods
⩥ Electro surgical procedures
1. Impression procedures
2. Temporary restorations & fabrication
66
Interactions between the gingiva and the margin of restorations, J Clin Periodontol 2003; 30: 379–385.

67. PERIODONTAL-
RESTORATIVEINTERRELATIONSHIP
Seven characteristics of restorations and partial dentures are
important from a periodontal point of view:
1. Margins of restorations
2. Contours
3. Occlusion
4. Materials
5. Bridge design
6. Design of Removable Partial Dentures
7. Procedures of Restorative Dentistry themselves.
67

68. 1) Margins of restoration: location of restorative margins is
determined by many factors
1.Esthetic concerns.
2.Need for increased retention form
3.Refinement of pre-existing margins.
4.Root caries.
5.Cervical abrasion
6.Root sensitivity.
68

69. ⩥ Orkin et al 1986 demonstrated that sub gingival
restorations had a greater chance of bleeding and
exhibiting gingival recession then supra gingival restoration
⩥ Waerhaug 1978 stated that sub gingival restorations are
plaque retentive areas that are inaccessible to scaling
instruments.
69
BENNANI V. et al The periodontal restorative interface: esthetic considerations. Periodontology 2000,
Vol. 74, 2017, 74–101

70. 2) Contours
⩥ Over contouring:
The most common error in recreating the contours of the
tooth in dental restorations is over contouring of the facial
and lingual surfaces, generally in the gingival third.
⩥ Under contouring
Apparently, under contouring is not nearly as damaging to
the gingiva as the over contouring.
70

71. 3) Occlusion
Restorations that do not conform to the occlusion
patterns of mouth cause occlusal disharmonies
This may be injurious to the supporting periodontal
tissues.
71
BENNANI V. et al The periodontal restorative interface: esthetic considerations. Periodontology 2000,
Vol. 74, 2017, 74–101

72. 4) Materials
⩥ Restorative materials are not themselves injurious to the periodontal
tissues.
⩥ The surface of restorations should be as smooth as possible to limit
plaque accumulation.
⩥ Resins are highly polishable, but have deficiencies in strength, porosity
and wear.
⩥ Glass ceramics and porcelain veneers offer a clear advantage over any
other type of restorative materials in the maintenance of gingival health.
⩥ There are clinical situations in which the full crown is indicated prior to
restoration. It fulfills requirements that can be met in no other type of
restoration.
72
The effect of cervical sub gingival restoration margins on the degree of inflammation of the
neighbouring gingiva, Schweiz 1974.

73. 5) Bridge design
⩥ The health of the tissues around fixed prostheses depends
primarily on the patient’s oral hygiene; the materials with
which bridges are constructed appear to make little difference.
⩥ Ridge lap pontics, the least desirable design.
⩥ Bridge design with the least effect on the periodontium is the
sanitary or hygienic pontic.
73

74. 6) Design of Removable Partial Dentures
⩥ Partial dentures favor the accumulation of plaque,
particularly if they cover the gingival tissue.
⩥ Can also lead to gingival inflammation
74

75. 75
7) Restorative dentistry procedures:

76. BIOLOGIC CONSIDERATIONS
CONTOUR
⩥ Convexity on facial & lingual surfaces: provides protection &
stimulation to supporting structures during mastication.
⩥ Becker and Kaldahl opined that the buccal and lingual crown contour
should be ‘flat’ and not ‘fat’, usually < 0.5 mm, wider than the CEJ.
⩥ Yondelis et al demonstrated that greater the amount of facial and
lingual bulge of an artificial crown, the more the plaque retained at the
cervical margins.
76

77. INTERPROXIMAL CONTACTS
⩥ There must be a positive contact relation mesially and distally of
one tooth with another in each dental arch.
⩥ The contact points should be located incisially or occlusally and
buccally.
⩥ Placements of broad contacts that can be harmful to
periodontium,
⊳ Labio Lingual Location
⊳ Occluso gingivally
⊳ Narrow Contact
⊳ Contact too far gingivally
⊳ Contact too far occlusally
⊳ Too far buccal/ lingual
⊳ Open Contact
77

78. EMBRASURES/SPILLWAYS
V shaped spaces originate at the proximal contact area
between adjacent teeth.
⩥ Functions
• Serve as spillways for escape of food during mastication
.
• Prevents forcing of food into contact area.
78

79. RESTORATION OVER HANGINGS
⩥ Overhanging restorations contribute to gingival
inflammation due to their retentive capacity for bacterial
plaque.
⩥ Gilmore and Sheiham 1971 illustrated interproximal
radiographic bone loss adjacent to posterior teeth with
overhanging restoration.
79

80. ⩥ Jeffcoat and Howell 1980 demonstrated a link to the severity of
the overhang and the amount of periodontal destruction. Based
upon radiographic evaluation of 100 teeth with overhang and 100
without, they reported greater bone loss around teeth with large
over hangs. The severity of bone loss was directly proportional to
the severity of the overhang.
⩥ Spinks et al 1986 demonstrated that a motor driven diamond tip is
faster for removing over hangs and led to smoother restorations
compared to Sonic Scalers and Curettes respectively.
80

81. MARGIN PLACEMENT AND BIOLOGIC WIDTH
⩥ Supragingival
⩥ Equigingival
⩥ Subgingival
81

82. a) Supragingival margin
• Least impact on the periodontium.
• Preparation of the tooth and finishing of the margin is easiest
• Duplication of the margins with impressions can be done with
ease.
• Fit and finish of the restoration and removal of excess material
is easiest
• Verification of the marginal integrity of the restoration is
easiest.
82

83. b) Equigingival margin
⩥ Previously thought to retain more plaque than supra &
sub gingival margins therefore results in greater
gingival inflammation.
83

84. c) Subgingival margin
⩥ Greatest biologic risk.
⩥ Not as accessible as supra- or equi- for finishing
procedures.
84

85. Biologic width
Kois proposed three categories of biologic width based on the
total dimension of attachment and the sulcus depth following
bone sounding measurements.
1. Normal crest: Commonly seen (85%) and stable gingival
tissues
2. High crest: Unusual finding(2%), occurs on interproximal
surface adjacent to edentulous site.
3. Low crest: 13% occurrence rate, more susceptible to
gingival recession
85

86. Importance of determining the crest category
Allows the operator to determine the optimal position of
margin placement, as well as inform the patient of the
probable long-term effects of the crown margin on gingival
health and esthetic
86

87. TREATMENT
87

88. SURGICAL CROWN LENGTHENING
⩥ Crown lengthening surgery is designed to increase clinical crown
length.
INDICATIONS
⩥ Inadequate clinical crown for retention due to extensive caries,
subgingival caries or tooth fracture,
⩥ Short clinical crowns.
⩥ Placement of sub gingival restorative margins.
⩥ Unequal, excessive or unaesthetic gingival levels for esthetics.
⩥ Planning veneers or crowns on teeth with the gingival margin
coronal to the cemeto enamel junction (delayed passive eruption).
⩥ Teeth with excessive occlusal wear or incisal wear.
⩥ Restorations which violate the biologic width.
⩥ Assist with impression accuracy by placing crown margins more
supragingivally.
88

89. Contraindications
⩥ Deep caries or fracture requiring excessive bone
removal.
⩥ Post surgery creating unaesthetic outcomes.
⩥ Tooth with inadequate crown root ratio (ideally 2:1 ratio
is preferred)
⩥ Non restorable teeth.
⩥ Tooth with increased risk of furcation involvement.
⩥ Unreasonable compromise of esthetics.
⩥ Unreasonable compromise on adjacent alveolar bone
support.
89

90. GINGIVECTOMY
⩥ External bevel gingivectomy
⩥ Internal bevel gingivectomy
90

91. APICALLY POSITIONAL FLAP SURGERY
Indication
⩥ Crown lengthening of multiple teeth in a quadrant or
sextant of the dentition, root caries, fractures.
Contraindication
⩥ Apical repositioned flap surgery should not be used during
surgical crown lengthening of a single tooth in the esthetic
zone.
91

92. ⩥ Sugumari et al. in a report on surgical crown lengthening with apical
repositioned flap with bone resection performed in the fractured
maxillary anterior teeth region, showed satisfactory results both in
terms of functional (restoring biologic width) and esthetic outcomes.
⩥ Most authors agree that a minimum distance of 3mm is required
from the osseous crest to the final restorative margin following a
crown – lengthening procedures to allow the margin to finish supra
gingivally (Bragger et al 1992).
92

93. ESTHETIC CONSIDERATIONS IN
GINGIVAL TISSUE MANAGEMENT
Ideal interproximal embrasure.
⩥ Houses gingival papilla without impinging on it.
⩥ Extend interproximal tooth contact to top of papilla –
no excess space to trap food or esthetically
displeasing.
⩥ Ideal interproximal tooth contact: 2-3 mm coronal to
epithelial attachment.
93

94. Restorative correction of open gingival embrasure.
⩥ Moving the contact to tip of papilla.
⩥ Direct bonded restorations:
⩥ Margins of restoration carried subgingivally 1-1.5 mm.
⩥ Designing emergence profile: moving contact point
towards papilla while blending contour into tooth below
tissue.
94

95. Indirect restorations:
⩥ Desired contour & embrasure form established in
provisional restoration.
⩥ Gingival tissues are allowed to adapt for 4-6 weeks with
temporary, before tissue contour information is relayed to
laboratory to be used in final restoration
95

96. 4. Management of periodontal
health in children: pediatric
dentistry and periodontology
interface
96

97. ⩥ Dental plaque, periodontal disease and
dental caries
97

98. ⩥ Diagnosis and management of periodontal
conditions in childhood
⊳ Plaque should be recorded using
disclosing agents, thus allowing
identification of sites where it may be
contributing to gingivitis and/or caries
98

99. ⩥ Good-quality posterior bitewing radiographs will detect
early enamel caries lesions, as well as inter- proximal
bone changes.
⩥ This allows preventive intervention, including home-
care advice, and possibly sealing or resin infiltration to
avoid cavitation of the tooth.
⩥ Maxillary and mandibular anterior occlusal radiographs
will also allow early detection of caries in the
interproximal incisor surfaces and bone changes in at-
risk individuals.
99

100. ⩥ Prevention and treatment of periodontal
conditions
100

101. ⩥ Periodontal conditions with a combined pediatric
dentistry and periodontology focus in childhood
⊳ Dental Trauma
⊳ Smoking and drug use in adolscence
⊳ Overweight, obesity, metabolic syndrome and
diabetes
⊳ Respiratory diseses
⊳ Asthama
⊳ COPD
101

102. ⩥ Periodontal implications with dental enamel
defects and other dental anomalies in
children and adolescents
102
Anterior view of a supernumerary tooth fused to the
labial aspect of the maxillary left central incisor.
Surgical sectioning of the supernumerary with guid
tissue regeneration can achieve healthy labial
periodontal support for the incisor.

103. 5. Role of maxillofacial
radiology in the diagnosis
and management of
patients with complex
periodontitis
103

104. ⩥ Two-dimensional modalities
⊳ Intra-oral radiography
⊳ Panoramic radiography
⩥ Volumetric modalities (three dimensional)
⊳ Panoramic tomosynthesis
⊳ Cone-beam computed tomography
104

105. 105

106. 6. The nexus between periodontics
and oral pathology
106

107. ⩥ Gingival lesions of developmental/ genetic origin
⊳ Hereditary gingival fibromatosis
⊳ Ligneous gingivitis
⊳ Gingival hamartomas
⩥ Gingival lesions of traumatic origin
⩥ Gingival lesions considered to have an immunologic origin
⊳ Lichen planus
⊳ Mucous membrane pemphigoid
⊳ Pemphigus vulgaris
⊳ Orofacial granulomatosis
107

108. ⩥ Drug-induced gingival lesions
⩥ Cysts, potentially neoplastic and neoplastic
gingival lesions
108

109. 7. Surgical management in
dentistry
109

110. ⩥ Surgical exposure of an impacted canine for
orthodontics
110

111. ⩥ Removal of mandibular tori
111

112. ⩥ Autogenous block bone grafting for dental
implants
112

113. SUMMARY and CONCLUSION
113

114. ⩥ Contemporary periodontal therapy has evolved to become more
interdisciplinary and increasingly involves complex treatments,
including soft-tissue- regenerative and bone-regenerative
procedures
⩥ Esthetic considerations are a significant contributing factor in the
management of prosthodontic cases and an interdisciplinary
approach is often necessary to achieve an optimal resul
114

115. ⩥ Therapeutic options frequently require an imaging modality
capable of providing a diagnostic osseous baseline and
facilitate quantification of smaller incre- ments of bony
change, both loss and additive, that are comparable over
time
⩥ The close and intricate relationship between the periodontal
tissues and the processes of tooth movement suggest that
adjunct orthodontic therapy may play an important role in
overcoming these problems.
115

116. ⩥ On the other hand, excessive movement of teeth beyond the
anatomical boundaries of the alveolar process is commonly
believed to contribute to further destruction of the periodontal
tissues
⩥ Oral health of children and adolescents mirrors their general
health. Because oral health care is often delivered in isolation
from general health care
⩥ Thus referring a patient to the other disciplines of dentistry
and medicine is an important and a major step in the dental
practice and also referral from the other branches of specialty
is also equally important for a comprehensive therapy.
116

117. REFERENCES

118. ⩥ Clinical Periodontology - Carranza 13th edition
⩥ Clinical Periodontology- Jan Lindhe, Thorklid Karring, Niklaus P
Lang. 6th edition.
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prosthodontics and periodontics. Periodontol 2000 2017: 74: 40–62.
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treatment on the periodontal tissues. Periodontol 2000 2017: 74:
140–157.
⩥ Bennani V, Ibrahim H, Al-Harthi L, Lyons KM. The periodontal
restorative interface: esthetic considerations. Periodontol 2000
2017: 74: 74–101.
118

119. ⩥ Drummond BK, Brosnan MG, Leichter JW. Management of
periodontal health in children: pediatric dentistry and periodontology
interface. Periodontol 2000 2017: 74: 158–167.
⩥ Rotstein I. Interaction between endodontics and periodontics.
Periodontol 2000 2017: 74: 11–39.
⩥ Rich A, Seo B, Parachuru V, Hussaini HM. The nexus between
periodontics and oral pathology. Periodontol 2000 2017: 74: 176–181.
⩥ Scarfe WC, Azevedo B, Pinheiro LR, Priaminiarti M, Sales MAO. The
emerging role of maxillofacial radiology in the diagnosis and
management of patients with complex periodontitis. Periodontol 2000
2017: 74: 116–139.
⩥ Tong DC. Surgical management in dentistry – the interdisciplinary
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surgery. Periodontol 2000 2017: 74: 168–175.
119

120. THANK-YOU