PERIODONTICS 1

Diagnosis and Examination

Periodontics is one of the focuses on the INBDE and so a strong foundation is essential to your success.
In this set of notes, we will review all of the periodontics concepts tested on the INBDE, including
diagnosis and examination, classi cations, plaque and bio lm, pathogenesis, treatment planning &
prognosis, non-surgical therapy, surgical therapy, adjunctive therapy, and prevention and maintenance.

1 Diagnosis
A - ename
Periodontics is a branch of dentistry dealing B - denti
with the periodontium. The periodontium C – alveolar bon
D - gingiv
includes alveolar bone, periodontal ligament, E - epitheliu
cementum, and gingiva, F – free gingival margi
G – gingival sulcu
H – gingival ber
Anatomical Terms I - PD
• Periodontal Ligament (PDL) – bers J - PD
between cementum and alveolar bone K – PD
L - cementu
• Alveolar Bone – bone that supports teeth
• Gingival Sulcus – potential space between
tooth and gingiva Figure 1.01 General dental anatomy
• Periodontal Pocket – pathologically
deepened gingival sulcus
• Gingival Margin – peak of gingiva
• Free Gingival Margin – gingiva border
• Free Gingival Groove – shallow linear
depression marking transition from free
gingiva to attached gingiva
• Attached Gingiva – keratinized gingiva
rmly attached to underlying bone
• Alveolar Mucosa – mucosa not bound to Figure 1.02 Anatomical terms of Gingiva

bone, non-keratinized
• Muco-gingival Junction – junction Periodontal Disease
between attached gingiva and alveolar Periodontal disease, also known as
mucosa periodontitis, is a complex condition that
• Vestibular Fold – transition fold between plays on the interaction between bacteria and
alveolar mucosa of periodontium and its host (the patient).
labial/buccal mucosa near the lip or cheek • Microbial plaque – the initiating factor of
periodontitis, accumulation of bacteria on
the tooth surface

INBDE Booster | Booster PrepTM

fi
L

fi
e

fi

fi

fi
 PERIODONTICS 2

There are 3 states of periodontal health 2 Examination

1. Periodontal Health – absence of
in ammation, PDL destruction, and bone Tooth Examination
destruction Teeth are examined for the following
2. Gingivitis – presence of in ammation, 1. Erosion – teeth eroded from acidic food/
absence of PDL destruction and bone drink or stomach acid
destruction absent 2. Abrasion – mechanical wear (ex.
3. Periodontitis – presence of in ammation, aggressive tooth brushing) resulting in loss
PDL destruction, and bone destruction of tooth structure
3. Abfraction – exural forces resulting in
Pathogenesis of periodontal disease has a
loss of tooth structure, usually in cervical
number of steps
areas
1. Sub-gingival plaque bacteria present
4. Attrition – occlusal wear from tooth-on-
microbial challenge (LPS, antigens, other
tooth contact
by-products)
5. Hypersensitivity – exposed root surfaces
2. In ammatory response by up-regulated
host immune system
Periodontal Examination
‣ Cytokines, prostaglandins, MMPs
The following are evaluated in the examination
‣ Leads to gingivitis
of the state of periodontal health
3. Tissue destruction when microbial
1. Alveolar bone loss – seen on radiograph
challenge is chronic or potent
but not as reliable
2. Gingival recession – shift of gingival
margin apically to expose root from CEJ to
gingival margin
3. Tooth mobility – indicates loss of
periodontal support
4. Suppuration – sign of many neutrophils in
periodontal pocket
5. Furcation – branching point of tooth roots;
can be seen with enough periodontal bone
loss

Periodontal Health can also be assessed with

Figure 1.03 Gum recession various measurements
1. Probing Pocket Depth (PPD) – gingival
The above image depicts the body trying to margin to base of pocket
protect itself by retreating its tissues from the 2. Clinical Attachment Loss (CAL) –
plaque and bacteria measures the position of the soft tissue to
the CEJ ( xed point)
3. Bleeding on Probing (BOP) – used to
measure in ammation of periodontal
tissues
‣ Seen when PPD or CAL is being taken

INBDE Booster | Booster PrepTM

fl
fl

fi
fl

fl

fl

fl

 PERIODONTICS 3


INBDE Pro Tip:
CAL = PPD + recession
• Rearrange this formula to calculate the
unknown variable
• Recession can be a negative value (ex. when
gingiva is swollen/high)

Furcation
A Furcation is branching point between tooth
roots
• Furcation involvement – bone loss at the
furcation area; can be achieved through ...
‣ Shortened root trunk (CEJ to furcation)
and roots
‣ Narrow distance between roots
(interradicular dimension)

Cervical enamel projection – enamel dips

towards the furcation where there should be
cementum; allows the periodontal apparatus
to detach more easily.

Figure 1.04 Cervical enamel projection

INBDE Booster | Booster PrepTM

 PERIODONTICS 4

Classi cations
1 Classi cations Glickman Classi cation (Furcation)
• Class 1 – pocket formation into the FLUTE,
There are several methods of clinically but not enough to expose furcation,
classifying periodontal health: incipient
• Class 2 – pocket formation into the
Miller Classi cation (for Mobility) FURCA, also known as cul-de-sac furcation
• Class 0 – normal tooth mobility, expect involvement
• Class 3 – through-and-through furcation
some give to the tooth due to the PDL
• Class 1 – slightly more mobility than normal • Class 4 – through-and-through furcation, it
• Class 2 – moderate mobility (≤1mm) displays a clear space that can be seen
• Class 3 – severe mobility (>1mm), vertical through
mobility into tooth socket is possible
Alveolar Bone Loss
• The typical distance from the alveolar crest
Hamp Classi cation (Furcation)
• Class 0 – no furcation involvement = 2mm
• Class 1 – <3mm horizontal furcation • The line connecting the alveolar crest
involvement should usually be parallel to line
• Class 2 – >3mm horizontal furcation connecting CEJs
• Bone height is best measured with
involvement
• Class 3 – through-and-through furcation bitewing radiographs
involvement (the probe can be it through)
Horizontal bone loss occurs when bone loss is
Hamp classi cation uses a Naber’s Probe for still parallel to the line connecting CEJs
measuring.
• Each section represents 3mm Vertical or angular occurs when bone loss is
• Ability to dip probe into furcation indicates not parallel to CEJ line; and is classi ed by the
furcation involvement number of bony walls remaining (infrabony
defects).
• 1-wall – hemiseptal shape wall
• 2-wall – crater shape, most common
‣ Loss of interseptal bone between two
teeth, buccal and lingual walls remain
• 3-wall – trough shape
• 4-wall – bone remains around the
circumference
‣ Termed exclusively for extraction sockets

Figure 2.01 Probe types

INBDE Booster | Booster PrepTM

fi

fi

fi
fi
fi

fi

fi

 PERIODONTICS 5

3. Consistency – brosis if gingivitis is

chronic

Plaque-Induced Gingival Disease

Plaque-Induced Gingival Disease is a common
type of gingival disease that is caused by the
Figure 2.02 Vertical bone loss interaction between plaque bacteria and host
immune cells

INBDE Pro Tip: Terms for infrabony defects are Modi ed/in uenced by
very popular on the INBDE. Make sure you 1. Medications
know them! ‣ calcium channel blockers, dilantin and
cyclosporine associated with drug
Miller Classi cation (Recession) induced gingival enlargement
Miller classi cation indicates the probability of ‣ oral contraceptives
regaining root coverage through a connective 2. Systemic factors
tissue graft procedure. *Note that the Miller ‣ endocrine (diabetes, pregnancy)
classi cation for mobility is a separate system. 3. Malnutrition
• Class I – gingival recession does not reach
mucogingival junction+ loss of interdental Non-Plaque Induced Gingival Disease
bone or soft tissue not present Non-Plaque Induced Gingival Disease
‣ 100% likelihood of full coverage via graft is the less common type; and can be a
since no interdental bone was lost response to ...
• Class II - gingival recession reaches or goes 1. Allergies
beyond mucogingival junction+ loss of ‣ restoration materials
interdental bone or soft tissue not present ‣ food
‣ 100% likelihood of full coverage via graft 2. Trauma
since no interdental bone was lost ‣ factitious
• Class III - gingival recession reaches or ‣ accidental
goes beyond mucogingival junction + loss ‣ iatrogenic damage – damage from
of interdental bone or soft tissue/or root dentist
coverage prevented by tooth 3. Infection
malpositioning ‣ bacterial
‣ Partial likelihood of coverage via graft ‣ viral
• Class IV - gingival recession reaches or ‣ fungal
goes beyond mucogingival junction + loss 4. Hereditary Gingival bromatosis – rm,
of interdental bone or soft tissue/or root non-hemorrhagic tissue

2 Gingivitis and Classi cations

Gingivitis can be identi ed by the 3 Cs

1. Color – redder from increased blood ow
2. Contour – in ammatory exudate and
edema
INBDE Booster | Booster PrepTM

fi
fi

fi
fl

fi
fl

fi

fi

fi
fi

fi

fl

 PERIODONTICS 6

3 Periodontal Disease 3. Necrotizing

‣ Either ANUG or ANUP (acute necrotizing
Traditionally, periodontal disease is classi ed ulcerative gingivitis/periodontitis)
using 3 different terms: distribution, severity ‣ Pseudomembrane, fever, fetid breath,
and type. blunted papillae
‣ Speci c to individuals who smoke, have
Distribution stress, smoking and immunosuppression
Distribution describes how many sites are are predisposed
affected. Each tooth has 6 sites (disto-facial,
mid-facial, mesio-facial, mesio-lingual, mid- Periodontitis can therefore be classi ed by a
lingual, disto-lingual). Therefore, each patient’s distribution-severity-type-disease, respectively.
• Ex. localized-moderate-chronic-
total amount of sites is the number of total
teeth x 6. periodontitis
• Ex. generalized-slight-aggressive-
1. Generalized - ≥ 30% of sites
2. Localized - < 30% off sites periodontitis

Severity Epidemiology
1. Slight – CAL = 1-2mm The following are a few common facts on the
2. Moderate – CAL = 3-4mm INBDE:
• Most common to least common
3. Severe – CAL ≥ 5mm
periodontitis: chronic > localized
Type aggressive > general aggressive >
1. Chronic Periodontitis refractory
4 • Most prevalent group to get periodontitis
‣ Slow, progressive bone destruction
‣ Destruction proportional to amount of are Mexican Americans, non-Hispanic Black
microbial deposits (plaque) Americans, and those who regularly smoke.
‣ Patient is clinically unhealthy (ex. smoker,
diabetic) 4 New AAP Periodontal Classi cation
‣ Modi ed by systemic issues
‣ Tends to be older in age
In 2017, the American Academy of
2. Aggressive Periodontitis
Periodontology created a new periodontal
‣ Fast bone destruction
classi cation system. The JCNDE recommends
‣ Destruction not proportional to amount
being familiar with the old and new
of microbial deposits
classi cations for the INBDE during this
‣ Patient is clinically healthy
transition period.
‣ Molar/incisor pattern in local version
The major change lies in the establishment of
where deeper pockets only seen in
four main categories of disease processes.
molars and/or incisors
1. Periodontal Health & Gingival Disease
‣ Familial aggregation
2. Periodontitis
‣ Tends to be of younger age
3. Peri-Implant Diseases and Conditions
4. Periodontal Manifestation of Systemic
Diseases and Developmental and Acquired
Conditions

INBDE Booster | Booster PrepTM

fi
fi
fi
fi

fi

fi

fi

 PERIODONTICS 7

After assessing the overall disease, its severity Staging

is determined by a process called staging.
Lastly, the disease will be assessed for risk
factors, therapeutic outcomes and rate of
progression in a step called grading.
Periodontal Health & Gingival Disease
• Generally healthy, soft and hard tissue
around teeth
• One or two sites may have some gingival
in ammation (minimum BOP < 10% of sites
and PD ≤ 3mm)
• Intact Periodontium (no attachment loss or
bone loss)
• Reduced Periodontium (can have previous
attachment loss or bone loss due to either:
history of periodontitis however currently
stable or no history of periodontitis if
patient had for example a crown
lengthening procedure)
‣ Patient has minimal BOP and PD ≤3mm)
Staging describes the severity, complexity
and extent of the disease; and is measured
from slight to severe in stages I through IV,
respectively. It is a static measurement that
measures the amount of destroyed or
damaged tissue due to periodontitis. There
can only be one stage per patient, so the most
severe applicable option is used.
• Severity – usually based on worst
interdental CAL site
1-2mm Stage I
3-4mm Stage II
≥5mm Stage III or IV
‣ Radiographic bone loss (RBL) can also be
considered

Coronal third Stage I

Gingivitis
• BOP, erythema, edema Coronal third Stage II
‣ Minimum BOP < 10% of sites
‣ PD ≤ 3mm At/past middle third Stage III or IV
• Periodontal stability (no progressive
attachment or bone loss) ‣ #of teeth lost from periodontitis can also
be considered
Periodontitis
• periodontal tissue is lost due to plaque No teeth lost Stage I
which causes host-mediated in ammation
• often deeper PD No teeth lost Stage II
• interproximal attachment loss
≤4 teeth lost Stage III

≥5 teeth lost Stage IV

INBDE Booster | Booster PrepTM

fl

fl

 PERIODONTICS 8

• Complexity - based on PD CAL or RBL

No loss over 5 years Grade A

≤4mm + horizontal bone loss Stage I
<2mm loss over 5 years Grade B
≤5mm + horizontal bone loss Stage II
≥2mm loss over 5 years Grade C
≥6mm + vertical bone loss + Stage III
furcation %RBL/Age

≥6mm + occlusal trauma + Stage IV <0.25 Grade A

bite collapse
0.25-1.0 Grade B
Automatic Stage Placement
>1.0 Grade C
Vertical bone loss ≥ 3mm Stage III
Phenotype
or IV
Plaque exceeds bone loss Grade A
Furcation involvement class II Stage III
or III or IV Plaque consistent with bone Grade B
loss
<20 teeth remaining Stage IV
Bone loss exceeds plaque Grade C
• Extent and Distribution – based on teeth
Smoking
involved. This measure does not receive a
stage, but a distribution pattern. Non-smoker Grade A

<10 cigarettes/day Grade B

<30% of teeth involved Localized
≥10 cigarettes/day Grade C
≥30% of teeth involved Generalized
Diabetes
Molar/Incisor Pattern – Classic
molars and/or incisors localized No diabetes Grade A
are exclusively involved aggressive HbA1c < 7.0% Grade B
periodontitis
HbA1c ≥ 7.0% Grade C
Grading C-Reactive Protein (marker of
Grading is a measure based on changes in ammation)
overtime as well as risk factors and
responsiveness to therapies. Each patient is <1 mg/L Grade A
given a grading from A to C based on several
1-3 mg/L Grade B
factors. Clinicians should initially assume grade
B, then shift to A or C if applicable. The 3 mg/L Grade C
grading may change over time.

INBDE Booster | Booster PrepTM

fl

 PERIODONTICS 9

Peri-Implant Health
• No signs of in ammation or BOP around
implants.
• Probing depths should be less than 5 mm

Peri-Implant Mucositis
• Visual signs of in ammation or BOP around
implants.
• Probing depths greater than the baseline
(compared to the previous year recording)
• No signs of progressive implant bone loss

Peri-Implantitis
• Visual signs of in ammation or BOP around
implants.
• Probing depths greater than the baseline
(compared to the previous year recording)
• Signs of progressive implant bone loss

INBDE Booster | Booster PrepTM

fl

fl
fl

 PERIODONTICS 10

Plaque and Bio lm

1 Plaque Dental Plaque Formation
1. Pellicle Formation
As previously stated, the presence of microbial ‣ Develops in seconds
plaque is an indication of periodontal disease. ‣ Pellicle – proline-rich proteins,
However, dental plaque is not homogenous glycoproteins + other components that
and has a complex composition depending on allow bacteria to attach
location and time.
2. Bacterial Adhesion & Attachment
Dental plaque is composed of the following: ‣ Occurs in minutes
1. Organic components ‣ Weak, reversible van der Waals and
‣ Polysaccharides, lipids, glycoproteins, electrostatic forces are used for initial
proteins adhesion
2. Inorganic components ‣ Strong irreversible interaction between
‣ Phosphorus, sodium, calcium potassium host pellicle receptors and adhesion
uoride molecules are used for rm attachment
3. Supra-gingival Components ‣ Primary (early) colonizers mostly
‣ Aerobic bacteria streptococcus and actinomyces bacteria
- Gram positive on early layers near - Feed on sugar and carbon from food
tooth eaten and saliva
- Gram negative on outer surface
‣ Components from saliva 3. Colonization and Plaque Maturation
4. Sub-gingival Components ‣ Occurs within 1-2 days
‣ Anaerobic bacteria ‣ Primary colonizers are strongly attached
- Early layers near tooth are gram and allow other bacteria to attach by
positive coronally and gram negative providing receptors via coadhesion
apically ‣ Facultative gram-positive switch to
- Outer surface near epithelium are gram anaerobic gram-negative once the bio lm
negative matures & bacteria grow
‣ Components from gingival crevicular uid ‣ Secondary (late) colonizers like P.
(GCF) Intermedia and T. Denticola feed on
amino acids more
‣ Fusobacterium nucleatum binds primary
INBDE Pro Tip: Saliva and GCF in uence the
regions they are in proximity to. Hence, saliva
to secondary colonizers; is a bridging
in uences supragingival components and GCF micro-organism
in uences subgingival components.

INBDE Booster | Booster PrepTM

fl
fl
fl

fi

fl

fi

fl
fi

 PERIODONTICS 11

• Red complex – linked to both BOP +

deeper PD
‣ P. gingivalis
‣ T. forsythia
‣ T. denticola
• Orange complex – precedes red complex
in periodontal pocket
‣ Fusobacterium
Figure 3.01 Plaque formation ‣ C. rectus
‣ P. intermedia
Bio lm
Major Bacteria for INBDE
Bio lm is an organized network of bacteria
1. A. Actinomycetemcomitans (blue
along with its associated nutrients, enzymes,
complex)
by-products, oxygen etc.
• Consists of uid channels that allow ‣ Gram-negative rod bacteria, immobile
passage of nutrients through plaque to ‣ Capnophilic
deeper bacteria ‣ Causes aggressive periodontitis
• Quorum sensing – bacteria communicate ‣ Contains lipopolysaccharide (LPS) which
is an endotoxin located in outer
within bio lm to stimulate the growth of
membrane of all gram-negative bacteria
favorable species to inhibit that of
unfavorable species ‣ Contains leukotoxin which kills
• Bacteria in the bio lm tend to be more leukocytes
resistant to antimicrobials compared to ‣ IgG cleaving protease
other bacteria such as free-swimming ‣ Contains collagenase which breaks down
collagen
bacteria

2. P. Gingivalis (red complex)

2 Microbial Complexes
‣ Gram-negative rod bacteria, immobile
‣ Causes chronic periodontitis
Bacteria can be arranged into groups or ‣ Gingipain is a protease which cleaves
complexes based on their characteristics. In host proteins
fact, different complexes correspond to ‣ Fimbriae is used for adherence
different locations in plaque. ‣ Contains Capsule, Collagenase,
Hemolysin

3. T. Denticola (red complex)

‣ Gram-negative spirochete bacteria,
mobile
‣ Causes ANUG/ANUP
‣ Contain a protease that breakdown
complement factors immunoglobulins &
collagen
‣ Invades epithelium & connective tissue

Figure 3.02 Microbial Complexes

INBDE Booster | Booster PrepTM
fi
fi

fi

fl

fi

 PERIODONTICS 12

4. T. Forsythia (red complex) 3 Local Factors

‣ Gram negative rod bacteria, immobile
In combination with the presence of plaque,
5. P. Intermedia (orange complex) local factors contribute to periodontal disease
‣ Gram-negative rod bacteria, immobile by promoting accumulation and retention of
‣ Causes pregnancy gingivitis additional plaque bacteria.

6. C. Rectus (orange complex) 1. Calculus

‣ Gram-negative rod, mobile ‣ Mineralized plaque
- Takes 1-14 days for mineral salts to
7. F. Nucleatum (orange complex) precipitate & form plaque
‣ Gram-negative rod bacteria, immobile ‣ Calculus does not irritate gingival tissues,
‣ Bridging micro-organism (link between but the layer of plaque on top of it is an
primary and secondary colonizers) irritant
‣ Supragingival calculus
8. Other Bacteria - White or yellow
‣ S. salivarius – most common oral bacteria - Mineralized by saliva near salivary duct
& found in tongue openings
‣ S. mutans – cause coronal caries ‣ Subgingival calculus
‣ Actinomyces – found in healthy gingiva - Dark
& cause root caries - Mineralized by GCF
‣ Pseudomonas & Staph – cause peri- ‣ Identi ed by an explorer or visually
implantitis ‣ Interproximal calculus can be visualized
on radiographs
Plaque Hypotheses
Over the course of history, different theories of
plaque and disease have been hypothesized.
Although the most accurate hypothesis is
currently the ecological hypothesis, it is good
to know all 3.

1. Nonspeci c – amount of plaque correlates Figure 3.03 Calculus

to disease severity (independent of which
bacterial species is present)
2. Speci c – disease is only caused by 2. Materia Alba
speci c bacterial species ‣ White curd-like matter that is made up of
3. Ecological – certain bacteria in unorganized bacterial accumulation,
combination with speci c host factors can desquamated epithelial cells, food debris,
shift the environment. This shift can favor salivary proteins
pathogenic bacteria

INBDE Booster | Booster PrepTM

fi
fi
fi

fi

fi

 PERIODONTICS 13
4. Malocclusion
‣ Plaque retention by crowding
‣ Mesial drifting of teeth due to missing
teeth can retain plaque and impact food

5. Faulty Restorations
‣ Overcontoured restorations can lead
Figure 3.04 Microbial Complexes
more plaque retention than
undercontoured restorations
3. Extrinsic Stains ‣ Plaque retention from overhanging
margins or rough surfaces
Color Association
6. Sub-gingival Margins
Orange Often associated with
‣ Associated with plaque accumulation and
anterior teeth,
gingival in ammation
Poor oral hygiene
‣ Can be seen even when margins are ideal
Brown Drinking dark
beverages, 7. Appliances
Poor oral hygiene ‣ Orthodontics
- Can increase plaque retention
Yellow-Brown Usage of stannous
- Can create excessive forces on
uoride of CHX
periodontium
Dark brown/ Tobacco use
Black 8. Oral jewelry
‣ Can lead to recession and bone loss
Green & Yellow Chromogenic bacteria
cause this stain 9. Removal Partial Dentures
Bluish-Green frequent exposure of ‣ Increase abutment teeth mobility
metallic dust ‣ Increase plaque accumulation

Black thin lines Found in healthy 10.Self-In icted Injury

on cervical third mouth and due to iron ‣ Excessive biting ngernails
consumption - Gingival tissue destruction
‣ Aggressively brushing horizontally

INBDE Pro Tip: Extrinsic tooth stains are mainly

an esthetic concern and usually do not in uence
gingival in ammation. However, they are
important to study as they are extremely
popular on the INBDE.

INBDE Booster | Booster PrepTM

fl
fl
fl
fl

fi

fl

 PERIODONTICS 14

Pathogenesis
Immune cells and enzymes play a crucial role in • T-cytotoxic (CD8) cells – kill intracellular
the pathogenesis of periodontal disease. antigens
Ultimately, they are responsible for the • NK cells – Like T cells, which detect &
destruction of periodontal tissue as a host destroy cells infected by virus
response to the plaque bacteria. There are
numerous cell types and proteins to consider. 2 Mediators

1 Immune Cells Pro-in ammatory - lead to tissue destruction

• IL-1 – mediate bone resorption
Neutrophils • IL-6
• First immune cells to respond • MMPs – break down collagen (primary
• Control bacterial challenge & release mediator in periodontal tissue destruction)
chemicals that destroy periodontal tissue
• Phagocytize and kill bacteria via Anti-in ammatory - oppose tissue
myeloperoxidase destruction
• Migrate to periodontal pocket via • IL-4
chemotaxis to prevent invasion of • IL-10
periodontal bacteria • TIMPs
• MMP-8 (neutrophils collagenase)
‣ Proteinase destroys periodontal tissue 3 Pathogenesis of Gingivitis
‣ Restricted by tetracycline
• Damaged neutrophil chemotaxis lead
Pathogenesis of Gingivitis
aggressive periodontitis
1. Initial Lesion (2‒4 days)
• Neutrophil activity too high and too low
‣ GCF increase
can lead to ! tissue destruction
‣ Neutrophil penetration
2. Early Lesion (4‒7 days)
Macrophages
‣ Increase collagen loss
• Antigen presenting cells (APCs)
‣ T-lymphocyte penetration
• Control immune response by releasing
‣ BOP
cytokines
3. Established Lesion (14‒21 days)
‣ B-lymphocytes penetration + plasma cells
Mast Cells
• IgE production ‣ Collagen loss, consistency change,
contour change, and clinical color change
• Vascular permeability and dilation
‣ Gingivitis becomes more established at
this stage
Lymphocytes
4. Advanced Lesion
• B-cells turn into plasma cells to produce
‣ Irreversible stage - the establishment of
antibodies
periodontal bone loss
• T-helper (CD4) cells – coordinate immune
response by activating other cells

INBDE Booster | Booster PrepTM

fl

fl

 PERIODONTICS 15

Treatment Planning & Prognosis

1 Treatment Planning Phase 2 – Surgical Phase
• When non-surgical phases are unsuccessful
• Treat with endodontics
Goals
• Remove periodontal pockets and
Short-Term Goals:
regenerate periodontal ligaments, x soft
• Decrease gingival in ammation by xing
and hard tissue defects
the causes
• Periodontal therapy such as implants
• More focus on comfort and esthetics
Phase 3 – Restorative Phase
Long-Term Goals:
• The stage at which periodontal disease is
• Stop hard and soft tissue destruction
controlled
• Stop pain
• Final restoration, xed or removable
• Stopping recurrence
prosthodontics
• Prevent tooth loss, but cannot always save
Phase 4 – Maintenance Phase
all teeth
• Also known as:
• Achieve occlusal function and stability
‣ Supportive periodontal therapy
• More focus on function and health
‣ Periodic ongoing evaluation of OHI and
condition of periodontal tissue
Phases of Periodontal Treatment
• Continued along with phases 2 & 3 every 3
Phase 0 – Preliminary Phase
months during the rst year
• Prior to starting treatment
• Emergency purposes
Risk Elements
• Extract hopeless teeth
Risk Factors – commonly result in disease:
‣ Bone loss involving apex of tooth
• Pathogenic bacteria
‣ Hardly any periodontal attachment that
• Diabetes
cannot be restored
• Smoking
Phase 1 – Non-Surgical Phase
• Microbial tooth deposits
• Plaque control, caries control, diet control
and patient education Risk Determinants – background
• Scaling & root planing, oral hygiene
characteristics that cannot be changed &
instruction, prophylaxis increase the possibility of disease
‣ Remove local factors • Age – older = longer time exposed to
• Antibiotics (local or systemic)
etiological factors
• Fix restorative irritation • Genetic factors – periodontitis has high
• Periodontal re-evaluation (PD,
inheritability (severe chronic periodontitis
in ammation) 4-8 weeks after phase I result due to IL-1 gene polymorphism)
therapy • Socioeconomic status – higher rate of
‣ Healing and formation of junctional smoking, less dental visits & awareness
epithelium • Gender – male CAL > female CAL

INBDE Booster | Booster PrepTM

fl

fi

fi

fl

fi
fi

 PERIODONTICS 16

Risk Indicators – not commonly result in Systemic Factors

disease, but could potentially put one at a • Diabetes
higher risk: ‣ Worse prognosis if poorly controlled and
• HIV/AIDS – the immunocompromised often not controlled
seen with ABUG/ANUP • Smoking
• Stress – mental stress can inhibit the ‣ increases periodontal disease frequency
immune system and severity
• Osteoporosis – decreased bone mass may ‣ Reduced healing ability to nonsurgical
progress of periodontal disease and surgical therapies
• Low dental visits • Parkinson’s Disease
‣ More dif cult to perform oral hygiene (ex.
Risk Marker or Predictors – disease that is reduced motor ability making it harder to
associated quantitatively (previous history) brush
• CAL – most important indicator
• BOP Anatomic Factors
• History of periodontal disease • Cervical enamel projections
• Tooth mobility – poorer response to
2 Prognosis therapy
• Root factors
‣ Root proximity
Prognosis is the anticipation of the probable
‣ Short, tapered roots
course of a disease. In dentistry, the entire
‣ Root concavities
mouth needs to be looked at before prognosis
• Furcation involvement – more dif cult to
of individual teeth can be done.
clean
• Bifurcation ridges
Clinical Factors
• Plaque control – poor oral hygiene
Prosthetic and Restorations
instruction
• Disease severity – CAL > PD These factors are indirectly related to
• Vertical bone loss – more favorable periodontal disease and can in uence the
prognosis of teeth:
prognosis than horizontal bone loss, since it
• Non-vital teeth
has the potential to be treated with
• Root resorption
regenerative therapy
• Abutment selection
• Age – younger patients have more time
• Caries
and opportunity for the disease to get
worse
• Low patient compliance

INBDE Booster | Booster PrepTM

fi

fl

fi

 PERIODONTICS 17

3 Prognosis Classi cation

There are 6 categories of prognosis classi cation. A category could be assigned to the whole mouth
or an arch.

Bone Level Clinical Factors Local Factors Systemic Cooperation

Factors

Excellent No bone loss None Gingival health No Good

Good Suf cient None Can be No Good

alveolar maintained
support

Fair Insuf cient Mobility, Can be Limited Adequate

alveolar furcation I maintained
support

Poor Moderate bone Mobility, Dif cult areas to Yes Questionable

loss furcation I or II maintain

Questionable Advanced bone Mobility, Inaccessible Yes Inadequate

loss furcation II or III areas

Hopeless Advance bone Extraction is Cannot maintain Uncontrolled Inadequate

loss recommended

INBDE Booster | Booster PrepTM

fi
fi
fi

fi
fi
 PERIODONTICS 18

Non-Surgical Therapy
1 Scaling and Root Planing

Scaling and root planing aim to remove the

etiologic factors of plaque and calculus in
order to restore gingival health.

Scaling – removes supra-gingival and sub-

gingival plaque and calculus

Figure 6.01 Scaler types

Root planing – removes residual embedded
calculus and rough cementum
3. Ultrasonic Scalers
Scaler Types i. Remove stubborn calculus
1. Sickle Scalers ii. Contraindicated for patients with:
‣ Remove supragingival calculus a. Pacemakers
‣ triangle cross-section b. Risk for respiratory disease
‣ two cutting edges – either edge can be c. Infectious disease that can be
used to remove and scrape off calculus transmitted via aerosols
2. Curettes iii. Several functions to clean pocket
‣ Remove subgingival calculus a. Acoustic turbulence creates
‣ rounded edge avoids trauma to gingival agitation that can breakdown
tissue bacterial cell walls
‣ Universal curettes – any area of the b. Flush out with water
mouth c. Vibration mechanically removes
- two cutting edges, semicircle cross- deposits
section d. Cavitation
‣ Gracey curettes – speci c areas of the iv. Piezoelectric ultrasonics
mouth a. vibrate in linear pattern
- One cutting edge, semicircle cross v. Magnetostrictive ultrasonics
section (Cavitron)
- Gracey 1-2 & 3-4 ! anterior a. Vibrate in elliptical pattern
- Gracey 5-6 ! anterior + premolars
- Gracey 7-8 & 9-10 ! posterior, facial/
lingual
- Gracey 11-12 ! mesial, posterior
- Gracey 13-14 ! distal, posterior

INBDE Booster | Booster PrepTM

fi

 PERIODONTICS 19

Strokes 2 Prophy Cup and Brush

1. Exploratory
‣ Light stroke for probes and explorers to Prophylaxis paste
detect CAL or pocket depth • Grittier than toothpaste
2. Ultrasonics • Used to remove extrinsic stain
‣ Light intermittent strokes Prophy Cup
‣ Tip instrument parallel to tooth • Flexes on light pressure
3. Root planing • Helps remove extrinsic stains and pocket
‣ Light to moderate pulling stroke used for access
smoothing Prophy Brush
4. Scaling • Enables greater access to occlusal grooves
‣ Stronger and shorter pulling stroke used and interproximal spaces
to remove hard deposits Prophy Jet
• Ejects water and sodium bicarbonate
Curette Angulation • Removes soft deposits and extrinsic stains
Curette angulation is speci c and changes
when you scale or root plane a tooth. The
angle referenced is between the tooth surface
and face of the instrument.
• 0 degrees (closed-angle) – during initial
insertion of curette into pocket
• 45-90 degrees (open-angle) – when
scaling and root planing the tooth
Essentially, you are facing the instrument
parallel to the tooth surface when inserting,
then angling when you start scaling.

Figure 6.02 Curette Angulation

INBDE Booster | Booster PrepTM

fi

 PERIODONTICS 20

Surgical Therapy
Surgical therapy is considered when non-
surgical therapies do not resolve the issue. The
ap technique is often used during surgery.
After surgery, post-operative plaque control is
essential.

1 Flap Incisions
Figure 7.01 Papilla preservation

Flap Design Flap Thickness

There is a certain shape that soft tissues should
be cut in order to access defective periodontal Split/Partial thickness (mucosal) ap
tissue safely. Includes gingiva/mucosa + submucosa
The following rules should be adhered to: • Mucogingival surgery
• Wider base apically to allow blood ow
‣ No need to expose bone
down to coronal part of ap (narrow base
would sever vasculature that feeds more Full thickness (mucoperiosteal) ap
coronal tissue) Includes mucosa + submucosa + gingiva +
• Avoid vital structures periosteum
• Incisions over intact bone • Periodontal regeneration & osseous
‣ Avoid bony defect and eminences surgery
• Round corners
‣ Allows primary closure and apically
• Flap margins contact tooth at line angle repositioned aps
• Alveolar bone exposure normally lead 1mm
Papilla Preservation bone resorption & remodeling
Papilla Preservation ap
• Incision that preserves the papilla Involves 3 horizontal incisions:
• Edges of ap contact line angles of tooth 1. Internal/reverse bevel
‣ ~1mm from gingival margin
Conventional ap ‣ opens pocket lining while preserving
• Incision that splits the papilla outer gingiva
• Could result in loss of papilla and black 2. Sulcular/crevicular
triangle ‣ From base of pocket to alveolar crest
2. Interdental/interproximal
3 options
‣ Removes collar of tissue around the tooth
• Lingual ! facial line angle
that was made during the previous two
• Lingual ! lingual line angle
incisions
• Facial ! facial line angle

INBDE Booster | Booster PrepTM

fl

fl

fl

fl

fl

fl

fl

fl

fl

 PERIODONTICS 21

2 Bone Graft Materials

Some surgeries include bone grafts as part of

the treatment. We need to review a few terms
describing these bone graft materials before
learning about speci c surgeries.
Figure 7.02 Horizontal incisions
Graft materials should carry out at least some
of the following principles:
Flap Types • Osteoconductive – scaffold (all bone grafts
• Modi ed Widman ap are osteoconductive)
‣ Allows sub-gingival access for • Osteoinductive – turns close by progenitor
debridement so that new attachment can cells into osteoblasts
form • Osteogenic – creates bone
‣ Uses the three horizontal incisions
There are 4 main categories of graft materials.
• Apically repositioned ap All grafts are osteoconductive.
‣ Includes vertical releasing incision beyond The type of graft is listed from most ideal to
mucogingival junction to reduce least ideal graft material:
periodontal pocket via moving gingival • Autograft – from the patient
margin apically ‣ Osteoconductive, osteoinductive and
osteogenic
• Allograft – from someone else, usually
cadaver
‣ Osteoconductive and osteoinductive
• Xenograft – from an animal, usually cow
• Alloplast - synthetic or inorganic

3 Categories of Surgery
Figure 7.03 Repositioned ap

Gingival Surgery
Periodontal Pack • Excision only involves gingiva and soft
• Used after invasive ap surgery tissue above the mucogingival junction
• Protects the surgical wound, maintains • healing by secondary intention (open
tissue placement, prevents bleeding, wound, walls do not suture together)
reduces discomfort
• Do not accelerate the healing There are two types of gingival surgery:
• Left in the mouth for 1 week • Gingivectomy
‣ To remove supra-bony pocket or gingival
enlargements (more aggressive therapy)
• Gingivoplasty
‣ To reshape tissue deformities (less
aggressive, addresses esthetic concerns)

INBDE Booster | Booster PrepTM

fi

fl
fl
fi

fl
fl

 PERIODONTICS 22

Distal Wedge Surgery • Connective tissue graft (CTG)

• Used for pocket reduction distal to the ‣ Placing a piece of connective tissue to
terminal molars suture over the exposed root surface
• Speci c type of gingival surgery ‣ Donor site needs to have enough
• Mandibular – full thickness ap + V-shape attached gingiva
incisions - Palate - most common donor site
• Maxillary – full thickness ap + parallel ‣ Harvested tissues is inner connective
incisions tissue only (not epithelium)
‣ Occurs coronal to gingival margin

Figure 7.04 Distal wedge surgery

Figure 7.05 CT graft

Mucogingival Surgery
Mucogingival surgery involves operating on
the gingiva and mucosa. There are several • Vestibuloplasty
types
‣ Deepens the vestibule
• Free gingival graft (FGG)
• Frenotomy
‣ Increase the amount of keratinized tissue
‣ Incision of the frenum
apical to gingival margin • Frenectomy
‣ Attached gingiva enhances plaque
‣ Removing the entire frenum
removal and minimizes in ammation
around abutment teeth and implants Osseous Surgery
‣ Achieving 2mm of attached gingiva is This type of surgery deals with the bone, thus a
recommended speci c assessment of the periodontal bony
‣ Donor site usually from palate architecture is performed for the detection of
‣ Graft thickness ideally 1-1.5mm bony detects and their severity.
‣ Free graft = transplant without a • Flat architecture
nourishing blood supply ‣ Interproximal and radicular bone heights
- Thus, need to expose vascular bed at are the same
recipient site to supply newly grafted • Positive architecture
tissue ‣ Interproximal bone is coronal to radicular
bone
‣ ideal alveolar bone morphology
• Negative architecture
‣ Inter-proximal bone is apical to radicular
bone

INBDE Booster | Booster PrepTM

fi

fi

fl
fl

fl

 PERIODONTICS 23

4 Healing Process

Mechanisms of Healing
• Regeneration
‣ Comeback to normal formation and
function
• Repair
‣ Not fully recovers formation and function
Figure 7.06 Osseous surgery
‣ Healing via scar formation or formation of
long junctional epithelium
• Reattachment
Osseous surgery has the aim of achieving
‣ Epithelial and connective tissue reconnect
positive architecture.
with root surface after incision or injury
• Ostectomy – removes supporting bone
• New Attachment
• Osteotomy – removes non-supporting
‣ Inserting new PDL bers into new
bone
cementum in areas with insuf cient
• Clinical crown lengthening – lowers bone
attachment
(osteotomy) to expose more tooth
‣ Combines with gingivectomy (when at
Wound Healing Cells
least 2 mm keratinized tissue after
From fastest to slowest, the following cells
gingivectomy) or with apically positioned
begin to populate the wound area:
ap
1. Epithelial cells
2. Connective Tissue cells
Periodontal Regeneration
3. Bone cells
• Guided Tissue Regeneration (GTR)
4. PDL cells
‣ Regenerates PDL, bone & cementum

3 components
• Barrier membrane – placed over defect
and allows hard tissue growth and prevents
soft tissue from growing in
• Bone graft – osteoinductive,
osteoconductive and /or osteogenic
• Biologic agent – promotes healing
environment for tissue formation

INBDE Pro Tip: The various periodontal

surgeries can be summarized into 2 methods.
Additive & Subtractive
• Periodontal regeneration (additive)
• CTG (additive) Figure 7.07 Wound healing cells
• FGG (additive)
• Coronally advanced ap (additive)
• Gingivectomy (subtractive)
• Apically positioned ap (subtractive)
• Resective osseous surgery (subtractive)
INBDE Booster | Booster PrepTM
fl

fl
fl
fi

fi

PERIODONTICS 24

Root Surface Treatment

• Chelating agents like EDTA can be used to
to stimulate new attachment by exposing
the collagen brils through
demineralization.

Defects and Treatments

• 1 and 2-wall defects
‣ Resection (ostectomy)
• 3 and 4-wall defects
‣ Regeneration

INBDE Booster | Booster PrepTM

fi

 PERIODONTICS 25

Adjunctive Therapy
Adjunctive therapy is used alongside surgical Local Delivery Antibiotics (LDA)
or non-surgical therapies to help aid in the • Used when conventional therapies still
healing process of periodontal disease. result in localized recurrent and/or residual
PD ≥5mm + in ammation
1 Antibiotics
Common Name Antibiotic
Antibiotics are used to target bacteria in the
Arrestin Minocyline
periodontal pocket that are the initiating factor
of plaque. Atridox Doxycyline
• Only use as an adjunct to phase I non-
PerioChip Chlorhexidane
surgical therapy during mechanical
gluconate
debridement
• Most often used for localized aggressive
periodontitis 2 Host Modulation Therapy
• Do not take bactericidal (killing) and
bacteriostatic (stopping growth) drugs at
As you know by now, tissue destroyed from
the same time
periodontal disease comes from the host
• Used for refractory periodontitis (disease
response to bacterial challenge. Thus, host
not resolved despite undergoing
modulation therapy aims to suppress the
treatment)
destructive nature of the host immune
response
The following are a few antibiotics to take note
• Use for chronic periodontitis (not
of:
aggressive)
Tetracyclines
• Only use as an adjunct to phase I
• In GCF
mechanical debridement
‣ GCF is found inside each pocket, thereby
targeting pocket bacteria
NSAIDs
• Doxycycline can help with patient
• Inhibits prostaglandins = inhibits
compliance
in ammation
‣ One dose per day
Bisphosphonates
Amoxicillin (AMX) + Metronidazole (MTZ)
• Inhibit osteoclasts = inhibits bone
• Most common and effective antibiotic
destruction
routine for periodontal disease
• Side effect - Bisphosphonate related oral
• AMX (500mg TID) + MTZ (200mg TID) for
necrosis of the jaw (BRONJ)
14 days
• Then length of duration is more bene cial
than the dose
• Do not mix MTZ and alcohol

INBDE Booster | Booster PrepTM

fl

fl

fi

 PERIODONTICS 26

Subantimicrobial Dose Doxycycline (SDD) 4 Furcation Correction

• Inhibits MMPs (collagenases) that destroy
the PDL Furcation involvement is very dif cult to clean
• Used systemically and locally
suf ciently, often leading to periodontitis.
• 20mg, twice/day for 3-9 months
Currently, there are 4 different treatment
‣ Subantimicrobial dose – less than normal options for furcation involvement.
dose if one had a bacterial infection
• Only one from this list approved by FDA +
Furcation Plasty
accepted by ADA • Opening furcation further up + smoothing
• Should be an adjunct to removing plaque
so that there is more access for cleaning

3 Occlusal Correction Tunneling

• Removing bone and moving soft tissue
Sometimes periodontal disease stems from apically to reveal more furcation for easier
malocclusion. Traumatic occlusion can cleaning access
create occlusal forces that exceed the
reparative ability of attachment apparatus. Root Amputation/Resection
For instance, heavy contact or interference • Cutting off and removing one root +
could injure the PDL. Occlusal indicating smoothing ! endodontic treatment !
wax or articulating paper can be used to place crown that leaves open space for
check for such occlusion. cleaning
• Commonly seen in removing distobuccal
Occlusal trauma can be divided into 3 roots of maxillary rst molar
categories
• Primary – too much pressure on normal Hemisection/Premolarization
periodontium • Cut molar in half ! creates 2 premolar-like
• Secondary – normal tooth-on-tooth teeth
contact but reduced periodontium
• Fremitus – teeth vibrate when closing

Occlusal therapies should be used as

treatment only after in ammation has resolved
• Interocclusal appliance (biteguard)
‣ Redistributes occlusal forces more evenly
• Occlusal adjustment (coronoplasty)
Figure 8.01 Furcation correction (1)
‣ Reshapes occlusal surface
• Splinting
‣ Immobilizes overly mobile teeth
‣ Increases comfort and function

INBDE Booster | Booster PrepTM

fi

fi
fl

fi

PERIODONTICS 27

Figure 8.02 Furcation Correction (2)

INBDE Pro Tip: There is only one prognosis

based periodontal question on the INBDE. If
you only choose to remember one thing, know
that CAL is the most important factor in
determining prognosis

INBDE Booster | Booster PrepTM

 PERIODONTICS 28

Prevention and Maintenance

1 Toothbrushing

Bass Method
• Regarded as best method of brushing
amongst examiners
• Place bristles at gingival margins at 45
degrees to the tooth sulcus
• Extend slightly subgingival in order to Figure 9.02 Flossing method
breakup plaque in the cervical area
3 Waterpik

Waterpik
• Made to ush out food debris with water
• Lowers bacterial load on gingiva
• Cannot remove bio lm on the tooth
surface = does not prevent periodontal
Figure 9.01 Toothbrushing method disease

Toothbrush
• Soft bristles are recommended as they do
not irritate the gingiva as much as hard
bristles
• Aggressive brushing or hard bristles result
in tooth abrasion and gingival recession

2 Flossing

Figure 9.03 Waterpik

Flossing
• Wrap oss around middle ngers, hold
between thumbs and index ngers
• Important to curve oss into C-shape
against the surface of tooth
• Gently rub oss up and down tooth surface
on each side
• Remember to oss the distal surface of the
posterior-most teeth

INBDE Booster | Booster PrepTM

fl

fl

fl

fl
fl
fi

fi

fi