Periodontics

What is Periodontics?

Periodontium:
1. Alveolar bone
2. PDL
3. Cementum
4. Gingiva (gums)
Normal Periodontium
 Periodontal Disease
• Microbial plaque is generally considered the
initiating factor
• Periodontal health= no inflammation + no PDL
and bone destruction
• Gingivitis= inflammation + no PDL and bone
destruction
• Periodontitis= inflammation + PDL and bone
destruction (CAL)
 Pathogenesis
1. Microbial challenge (LPS, antigens) presented by
subgingival plaque bacteria
2. Upregulated host immune-inflammatory
response (cytokines, prostaglandins, MMPs)
3. Tissue destruction
 Tooth Exam
• Erosion—caused by acidic foods/beverages or
gastric acid
• Abrasion—loss of tooth structure by mechanical
wear
• Attrition—occlusal wear from functional contacts
with opposing teeth
• Abfraction—loss of tooth structure in cervical
areas due to tooth flexure
• Hypersensitivity—as a result of exposure of
dentinal tubules in root surfaces
 Periodontal Exam
• Probing pocket depth (PPD)—from gingival margin to base
of pocket
• Clinical attachment loss (CAL)—from CEJ to base of pocket
• Bleeding on probing (BOP)—best measure of inflammation
in periodontal tissues

PPD= 6mm

CAL= 6mm

BOP +
 Periodontal Exam

PPD= 4mm PPD= 6mm PPD= 9mm

CAL= 6mm CAL= 6mm CAL= 6mm

CAL= PPD + recession

 Periodontal Exam
• Gingival recession—from CEJ to gingival margin,
exposure of root surface due to apical shift of
gingival margin
• Alveolar bone loss—radiographic measure, but
not reliable
• Suppuration—indicates large number of
neutrophils in pocket
• Mobility—due to loss of periodontal support,
traumatic occlusion, or combination of both
• Furcation—bone loss at the branching point of a
tooth root
 Oral Exam
• Home care à plaque, calculus
• Inflammation à redness, swelling, BOP
• Destruction of periodontal tissues à PPD,
CAL, alveolar bone loss, mobility, furcation
involvement
Periodontics
 Miller Classification (Mobility)
• Class 0 normal physiologic mobility
• Class 1 slightly more than normal
• Class 2 moderately more than normal (≤1mm)
• Class 3 severely more than normal (>1mm) and
can be vertically depressed in socket
 Furcation
• Furcation= branching point of a tooth root
• Furcation involvement= an area of bone loss
at the furcation
 Furcation Factors
• Certain factors can predispose a tooth to
furcation involvement:
– Short root trunk
– Short roots
– Narrow interradicular dimension
– Cervical enamel projection
 Hamp Classification (Furcation)
• Class 0 no furcation involvement
• Class 1 horizontal furcation involvement <3mm
• Class 2 horizontal furcation involvement >3mm
• Class 3 through-and-through furcation
involvement

Nabers probe
Glickman Classification (Furcation)
• Class 1 pocket formation into the FLUTE, incipient
• Class 2 pocket formation into the FURCA, cul-de-
sac
• Class 3 through-and-through furcation lesion
• Class 4 through-and-through furcation lesion that
you can see through
 Alveolar Bone Loss
• Normal distance from CEJ to alveolar crest is
2mm
• Crest should be parallel to line connecting CEJs of
adjacent teeth
• Horizontal—stays parallel to line connecting CEJs
• Vertical or angular—classified by number of bony
walls remaining
 Infrabony Defects
• 1 wall hemiseptal
• 2 wall crater (most common)
• 3 wall trough
• 4 wall circumferential (extraction socket)
 Miller Classification (Recession)
• Determines likelihood of regaining root coverage
 Gingivitis
• Color= increased blood flow
• Contour= inflammatory exudate and edema
• Consistency= chronic gingivitis leads to fibrosis
 Plaque-Induced Gingival Diseases
• Most common
• Result of interaction between plaque bacteria and
inflammatory cells of host
• Modified by systemic factors
– Endocrine changes (puberty, pregnancy, diabetes)
– Blood dyscrasias (leukemia)
• Modified by medications
– DIGE with CCBs, dilantin, and cyclosporine
– Oral contraceptives
• Modified by malnutrition
– Vitamin C deficiency (scurvy)
 Non-Plaque-Induced Gingival Diseases
• Less common
• In response to infections
– Bacterial infections (Neisseria gonorrhoeae, Treponema pallidum)
– Viral infections (herpes)
– Fungal infections (candidiasis)
• In response to allergy
– Foods
– Restorative materials
– Toothpastes (sodium lauryl sulfate)
• In response to trauma
– Factitious= unintentionally produced
– Iatrogenic= caused by doctor
– Accidental= damage through burns from hot foods and drinks
• Hereditary gingival fibromatosis= non-hemorrhagic and firm
 Periodontal Disease (Severity)
Slight Moderate Severe
• 1-2mm CAL • 3-4mm CAL • ≥5mm CAL
Periodontal Disease (Distribution)
Localized Generalized
• <30% of sites • ≥30% of sites
 Periodontal Disease (Type)
Chronic Periodontitis Aggressive Periodontitis
• Clinically not healthy • Clinically healthy
• Slower, progressive bone • Rapid bone destruction
destruction
• Familial aggregation
• Microbial deposits
consistent with extent of • Microbial deposits not
destruction consistent with extent of
• Modified by systemic destruction
issues • Localized version has first
molar/incisor
presentation
 Periodontal Disease (Type)
Necrotizing (ANUG, ANUP)
• Pseudomembrane
• Fetid breath
• Blunted papillae
• Fever
• Predisposing factors are stress, smoking, and
immunosuppression
Periodontal Disease
Periodontics
Dental Plaque Composition
 Dental Plaque Composition
• Supragingival= aerobic
– Tooth= G+
– Outer surface of plaque= G-
• Subgingival= anaerobic
– Tooth= G+ coronal and G- apical
– Epithelium= G-
 Dental Plaque Composition
• Organic constituents—polysaccharides,
proteins, glycoproteins, and lipids
• Inorganic constituents—calcium, phosphorus,
sodium, potassium fluoride
• Supragingival components derive from saliva,
subgingival components derive from GCF
 Dental Plaque Formation
1. Pellicle Formation
– Within seconds
– Consists of glycoproteins, proline-rich proteins,
and other molecules that serve as attachment
sites for bacteria
 Dental Plaque Formation
2. Adhesion and Attachment of Bacteria
– Within minutes
– Initial adhesion is due to weak reversible van der
Waals and electrostatic forces
– Firm attachment is due to strong irreversible
interactions between specific bacterial adhesin
molecules and host pellicle receptors
 Dental Plaque Formation
3. Colonization and Plaque Maturation
– Within 24 to 48 hours
– Firmly attached primary colonizers provide new
receptors for attachment of other bacteria in a
process called coadhesion
– As bacteria grow and the biofilm matures, there is
a shift from facultative gram-positive to anaerobic
gram-negative
 Phases of Specific Bacteria

Fusobacterium nucleatum

Secondary (late) colonizers

Primary (early) colonizers

Pellicle
 Biofilm
• Fluid channels run through the plaque mass permitting
the passage of nutrients
• Quorum sensing refers to communication among
bacteria in a biofilm to encourage growth of beneficial
species and discourage growth of competing species
• Biofilm bacteria are more resistant to antimicrobials
than planktonic or free-swimming bacteria
Microbial Complexes
 Microbial Complexes
• Red complex is associated with BOP and deeper
pockets
– P. gingivalis
– T. denticola
– T. forsythia
• Orange complex precedes presence of red
complex supporting sequential nature of plaque
maturation
– Fusobacterium
– Prevotella intermedia
– Campylobacter rectus
 Plaque Hypotheses
• Non-specific= more plaque means more
disease no matter what bacterial species
• Specific= only specific bugs cause disease
• Ecological= mouth is an ecosystem just like a
rainforest, so certain bacteria and host factors
like smoking and diabetes change the
environment to favor pathogenic bacteria
 A. Actinomycetemcomitans
• Aggressive periodontitis
• Nonmotile, gram-negative rod
• Capnophilic—grows well in carbon dioxide
environment
• Leukotoxin—kills human neutrophils, monocytes,
and lymphocytes (toxic to leukocytes)
• Lipopolysaccharide (Endotoxin)—component of
all gram-negative outer membranes
• Collagenase
• Protease that cleaves IgG
 P. Gingivalis
• Chronic periodontitis
• Nonmotile, gram-negative rod
• Fimbriae—important in adherence
• Capsule
• Gingipain—protease that cleaves host
proteins
• Collagenase
• Hemolysin
 T. Denticola
• ANUG/ANUP
• Motile, gram-negative spirochete
• Penetrates epithelium and connective tissue
• Protease that can degrade collagen,
immunoglobulins, and complement factors
 T. Forsythia
• Nonmotile, gram-negative rod
• Protease that cleaves immunoglobulins and
complement factors
 P. Intermedia
• Pregnancy gingivitis
• Nonmotile, gram-negative rod
• Become darkly pigmented when grown on
blood agar plates
 C. Rectus
• Motile, gram-negative rod
• Polar flagellum
 F. Nucleatum
• Nonmotile, gram-negative rod
• Induces apoptosis of leukocytes and release of
tissue-damaging substances from leukocytes
 Other Bacteria to Know
• Actinomyces à healthy gingiva, root caries
• S. mutans à coronal caries
• S. salivarius à most common oral bacteria,
resides on tongue
• Pseudomonas, Staph à implants
Periodontics
 Calculus
• Mineralized dental plaque
• Precipitation of mineral salts into plaque usually occurs within 1-14 days
• Although calculus does not serve as a mechanical irritant to gingival
tissues, it is always covered with a layer of bacterial plaque which serves
as the primary irritant
• Supragingival= white/yellow, mineralization via saliva, occurs near salivary
duct openings
• Subgingival= dark, mineralization via GCF
• Calculus can be detected visually (especially with air) or with an explorer
• Interproximal calculus deposits can be detected radiographically
 Materia Alba
• Soft white cheeselike unorganized
accumulation of bacteria, salivary proteins,
desquamated epithelial cells, and occasional
food debris
• Easily displaced with water spray
 Extrinsic Stains
• Do not contribute to gingival inflammation and are
primarily an esthetic concern
• Orange= usually on anterior teeth, poor OH
• Brown= drinking dark-colored beverages, poor OH
• Dark brown and black= tobacco
• Yellow-brown= CHX and stannous fluoride
• Black= thin lines on cervical third, found in healthy
mouths, consumption of iron
• Green and yellow= usually on anterior teeth, poor OH
and chromogenic bacteria
• Bluish-green= occupational exposure of metallic dust
 Malocclusion
• Crowding can contribute to plaque retentive
areas
• Prominent roots and teeth associated with
high frena often experience gingival recession
• Mesial drift or extrusion associated with
missing teeth can lead to food impaction and
plaque retention
 Faulty Restorations
• Overhanging margins, open margins, rough
surfaces, open contacts can all create an
environment conducive to plaque retention
• Overcontoured restorations are worse for
gingival health than undercontoured
restorations
 Subgingival Margins
• Even when not faulty they are associated with
plaque accumulation, gingival inflammation,
and deeper pockets
 Appliances
• RPDs may result in increased mobility of
abutment teeth and increased plaque
accumulation
• Orthodontic therapy has also been shown to
increase plaque retention and can create
excessive forces on the periodontium
• Periodontal health must be established before
initiating orthodontic therapy
• Oral jewelry can also result in recession, pocket
formation, and bone loss
 Self-Inflicted Injury
• Aggressive horizontal brushing can cause
tooth abrasion and gingival recession
• Improper use of toothpicks and fingernail
biting can damage gingival tissues
Periodontics
 Neutrophils
• First line of defense
• Most important cells involved in controlling the bacterial challenge
and destroying periodontal tissue via release of destructive
molecules
• Migrate from subepithelial vascular plexus into the periodontal
pocket by directed locomotion called chemotaxis where they form a
barrier to protect the body from periodontal bacteria
• They internalize bacteria via phagocytosis and kills them using
“biologic bleach” of myeloperoxidase and oxygen radicals
• MMP-8 (neutrophil collagenase)= most important proteinase
involved in destruction of periodontal tissues, inhibited by
tetracyclines
 Neutrophil Abnormalities
• Defective neutrophil chemotaxis leads to
aggressive periodontitis
• It’s a lose-lose situation—too much neutrophil
activity leads to self-inflicted tissue destruction,
and too little neutrophil activity leads to
unchecked microbial challenge which also leads
to tissue destruction
• Neutrophil abnormalities include neutropenia,
Chediak-Higashi syndrome, Papillon-Lefevre
syndrome, and LAD-1 and LAD-2
 Macrophages Mf

• Antigen-presenting cells (APCs) like monocytes

and dendritic cells
• Regulate immune response via cytokine
release like IL-8
 Mast Cells Mast

• Vascular permeability and dilation

• IgE
 Lymphocytes
B
• B cells become plasma cells and make
antibodies
• T helper cells (CD4) help in Th
communication
• T cytotoxic cells (CD8) kill intracellular
antigens CTL
• NK cells are T cells that can recognize
and kill tumor and virally-infected cells
 Proinflammatory Mediators
• IL-1= bone resorption
• IL-6
• PGE2
• TNFa= macrophage activation
• MMPs= collagen destruction
Protein-ase à eats proteins
 Anti-inflammatory Mediators
• IL-4
• IL-10
• TIMPs
 Pathogenesis of Gingivitis
• Stage 1, Initial Lesion—2 to 4 days, neutrophil
infiltration, increased GCF
• Stage 2, Early Lesion—4 to 7 days, T lymphocyte
infiltration, increased collagen loss, BOP
• Stage 3, Established Lesion—14 to 21 days, B
lymphocyte infiltration including mature plasma
cells, collagen loss, clinical changes in color,
contour, and consistency
• Stage 4, Advanced Lesion—transition to
irreversible damage of periodontitis
Periodontics
 Short-Term Goal
• Reduce gingival inflammation by correcting
conditions that cause it
 Long-Term Goals
• Eliminate pain
• Arrest hard and soft tissue destruction (CAL)
• Establish occlusal stability and function
• Reduce tooth loss—NOT designed to save all
teeth
• Prevent disease recurrence
 (0) Preliminary Phase
• Treat emergencies
• Extract hopeless teeth
 (1) Non-Surgical Phase
• Plaque control and patient education
• Diet control
• Caries control
• Prophylaxis, SRP, OHI to remove local
factors
• Correct restorative irritational factors
• Local or systemic antibiotics
• Periodontal re-evaluation (pocket
depths, inflammation) should occur
4-8 weeks after the completion of
phase I therapy to allow for healing
and formation of JE
 (2) Surgical Phase
• Reduce or eliminate periodontal pockets,
correct soft and hard tissue defects,
regenerate periodontal tissues, or place
implants
• Periodontal therapy, including placement of
implants
• Endodontic therapy
 (3) Restorative Phase
• Final restorations
• Fixed and removable prosthodontics
 (4) Maintenance Phase
• Also called supportive periodontal therapy,
periodic ongoing evaluation of OHI and
condition of periodontal tissues
• Periodontal maintenance performed in a
continuum with phase II and phase III therapy
every 3 months for the first year
 Risk Elements
• Risk factor= causally associated with the disease
(smoking leads to periodontal disease)
• Risk determinant= unchangeable background
characteristics, increases likelihood of disease
(gender, genetics)
• Risk indicator= not causally associated with the
disease (stress, osteoporosis may influence
periodontal disease)
• Risk marker or predictor= quantitative association
with disease (previous history, attachment level)
 Risk Factors
• Smoking
• Diabetes
• Pathogenic bacteria
• Microbial tooth deposits
 Risk Determinants
• Genetic factors—periodontitis may be
heritable, polymorphisms in IL-1 genes may
contribute to severe chronic periodontitis
• Age—due to prolonged exposure to etiologic
factors rather than the actual aging process
• Gender—males have more CAL than females
• Socioeconomic status—decreased dental
awareness, frequency of dental visits, and
more smoking
 Risk Indicators
• HIV/AIDS—ANUG/ANUP is more often seen in
immunocompromised individuals
• Osteoporosis—reduced bone mass may have
an impact on progression of periodontal
disease
• Infrequent dental visits
• Stress—emotional stress may interfere with
normal immunologic function
 Risk Markers
• Previous history of periodontal disease
• BOP
• CAL
Periodontics
 Prognosis
• Prognosis is the prediction of the outcome of
a disease
• Prognosis for individual teeth must be
considered in the context of the entire
dentition
 Clinical Factors
• Age—younger patient with the same level of
disease as an older patient has a worse prognosis
• Disease severity—CAL is more important than
PPD
• Plaque control—poor OHI
• Patient compliance—noncompliant and
uncooperative
• Vertical bone loss has a better prognosis than
horizontal bone loss because it can potentially be
treated with regenerative therapy (especially 3-
wall defect)
 Systemic Factors
• Smoking—smokers have increased prevalence
and severity of periodontal disease and
decreased healing response to both
nonsurgical and surgical therapy
• Diabetes—poorly controlled diabetes has
worse prognosis than well-controlled diabetes
• Parkinson’s—compromise the patient’s ability
to perform oral hygiene
 Local Factors
• Plaque and calculus
• Subgingival restorations—may contribute to
plaque retention
 Anatomic Factors
• Short, tapered roots
• Cervical enamel projections
• Enamel pearls
• Bifurcation ridges
• Root concavities—mesial of maxillary first premolar
• Developmental grooves
• Root proximity
• Furcation involvement—more difficult to clean (as is
true for many of these)
• Tooth mobility—do not respond as well to therapy
• Developmental grooves
 Prosthetic and Restorative Factors
• Abutment selection
• Caries
• Nonvital teeth
• Root resorption
 Prognosis Classification
BONE LEVEL CLINICAL FACTORS LOCAL FACTORS SYSTEMIC FACTORS PATIENT
COOPERATION

EXCELLENT No bone loss None Gingival health No Good

GOOD Adequate alveolar None Potential to No Good
support maintain

FAIR Inadequate alveolar Mobility, furcation I Potential to Limited Adequate

support maintain

POOR Moderate bone loss Mobility, furcation I Difficult areas to Yes Questionable
or II maintain

QUESTIONABLE Advanced bone loss Mobility, furcation Inaccessible areas Yes Inadequate
II or III

HOPELESS Advanced bone loss Extraction indicated Unable to maintain Uncontrolled Inadequate

CAL is the most important factor in determining the prognosis!

Periodontics
 Scaling and Root Planing
• Scaling= removal of both supragingival and
subgingival plaque and calculus
• Root planing= removal of embedded calculus
and rough cementum
• Primary objective is to restore gingival health
by removing these etiologic factors
 Sickle Scalers
• For supragingival calculus
• Two cutting edges
• Triangle in cross section
 Curettes
• For subgingival calculus
• Universal curettes can be used in any area of the mouth
– Two cutting edges
– Semicircle in cross section
• Gracey curettes adapt to specific areas of the mouth
– One cutting edge
– Semicircle in cross section
– Gracey 1-2 and 3-4—anterior
– Gracey 5-6—anterior and premolars
– Gracey 7-8 and 9-10—posterior, facial and lingual
– Gracey 11-12—posterior, mesial
– Gracey 13-14—posterior, distal
 Ultrasonic Scalers
• For tenacious calculus
• Contraindicated for patients with pacemakers, infectious diseases spread
by aerosol, and at risk for respiratory disease
• Magnetostrictive ultrasonics (Cavitron) vibrate in an elliptical pattern
• Piezoelectric ultrasonics vibrate in a linear pattern
• Ultrasonics have several functions to clean the pocket:
– Lavage—flush with water
– Cavitation—vacuum air bubbles collapse and release energy to flush debris
– Vibration—mechanically removes deposits and debris
– Acoustic turbulence—agitation observed in fluids by mechanical vibrations
that disrupts bacterial cell walls
 Strokes
• Exploratory—light feeling stroke used with probes and explorers
• Scaling—short, strong pull stroke to remove hard deposits
• Root planing—light to moderate pull stroke used for final smoothing
• Ultrasonics—light intermittent strokes with tip parallel to the tooth
surface and in constant motion
• When initially inserting a curette into the pocket, angulation between the
blade and the tooth should be 0 degrees (closed-angle) and when scaling
and root planing, this angulation is changed to 45-90 degrees (open-angle)
 Prophy Cup and Brush
• Cup flexes on slight pressure to the contours
of teeth to help in extrinsic stain removal and
pocket access
• Brush enables better access to select occlusal
grooves and interproximal areas
 Prophy Jet
• Delivers slurry of water and sodium
bicarbonate to remove extrinsic stains and
soft deposits
Periodontics
 Flap Design
• Wider base to ensure
adequate blood supply
• Incisions over intact bone, not
over bony defects or
eminences
• Rounded corners
• Vertical releases at line angles
• Avoid vital structures
• Post-operative plaque control
is the most important
procedure after periodontal
surgery
 Flap Thickness
• Split or partial thickness (mucosal) flap
– Gingiva/mucosa, submucosa
– Used for mucogingival surgery because
exposing the bone is unnecessary
• Full thickness (mucoperiosteal) flap
– Gingiva/mucosa, submucosa, periosteum
– Used for osseous surgery and periodontal
regeneration to permit primary closure as
well as in apically repositioned flaps
• Whenever alveolar bone is exposed like in
full thickness flaps, expect about 1mm of
bone resorption and remodeling
 Papilla Preservation
• Conventional flap= split the papilla
• Papilla preservation flap= preserve the papilla
 Full Thickness Flap
• Involves three horizontal incisions:
– Internal or reverse bevel—about 1mm from
the gingival margin, removes pocket lining
yet conserves outer gingiva
– Sulcular or crevicular—through base of
pocket to alveolar crest
– Interdental or interproximal—removes the
collar of tissue around the tooth you
created with the first two incisions
• Modified Widman flap involves these three
incisions and provides access to subgingival
areas for debridement with the goal of new
attachment
• Apically repositioned flap requires
additional vertical releasing incisions made
beyond the mucogingival junction in order
to attain pocket reduction
 Periodontal Pack
• Usually consists of ZOE
• Leave in place for 1 week
• Packs are placed to protect the surgical
wound, minimize discomfort, maintain tissue
placement, and help prevent post-op bleeding
• Packs do NOT enhance healing
 (1) Gingival Surgery
• Gingivectomy= excision of gingiva to eliminate
suprabony pockets or gingival enlargements
• Gingivoplasty= excision of gingiva to reshape
tissue deformities
• Healing is by secondary intention because
there is no tissue to approximate
 Distal Wedge
• Pocket reduction distal to terminal molars
• Maxillary= full thickness flap with parallel
incisions
• Mandibular= full thickness flap with V-shaped
incisions
 (2) Mucogingival Surgery
• Free gingival graft= widen
band of keratinized tissue
• Connective tissue graft= root
coverage
• Frenectomy= complete
removal of frenum
• Frenotomy= incision of
frenum
• Vestibuloplasty= deepen the
vestibule
 Free Gingival Graft
• No minimum width of attached gingiva has been
established, but 2mm is a good amount
• Attached gingiva helps enhance plaque removal
(less painful brushing), improves esthetics, and
reduces inflammation around abutment teeth
and implants
• Ideal thickness of graft is 1-1.5mm
• A “free” graft by definition is transplanted
without a nourishing blood supply so it must
undergo revascularization from the recipient bed
 Connective Tissue Graft
• Harvest the inner connective tissue only and
not the epithelium so it is less painful for
patients during healing
• Donor sites should always have enough
attached gingiva
• Palate is most common donor site for both
FGG and CTG
 (3) Osseous Surgery
• Visualization of bony architecture
allows clinician to determine the types
of bony defects that are present and
the extent of those defects
• Positive architecture= interproximal
bone is coronal to radicular bone,
normal ideal alveolar bone
morphology
• Flat architecture= interproximal and
radicular bone are at same height
• Negative architecture= interproximal
bone is apical to radicular bone
 (3) Osseous Surgery
• Ostectomy= removal of supporting bone
• Osteotomy= removal of non-supporting bone
• After ostectomy, peaks of bone often remain at
the line angles called widow’s peaks which
predispose to periodontal pockets in these areas

Clinical crown lengthening (CCL)

 Mechanisms of Healing After Surgery
• Regeneration= completely restore architecture
and function
• Repair= not completely restore architecture and
function, involving healing by scar or formation of
long JE
• Reattachment= reunion of epithelial and
connective tissue with root surface after incision
or injury
• New attachment= embedding of new PDL fibers
into new cementum that has been previously
deprived of its original attachment
 (4) Periodontal Regeneration
• Guided Tissue Regeneration (GTR)= regenerate bone,
cementum, and PDL
• Barrier membrane is the “tank”—prevents soft tissue
downgrowth and permits hard tissue ingrowth
• Bone graft is the “damage”—osteoconductive,
osteoinductive, and/or osteogenic
• Biologic agent is the “healer”—creates an environment
conducive to tissue formation
 Wound Healing
• These cells populate a wound area during the
healing process from fastest to slowest:
– Epithelial cells (1)
– CT cells (2)
– PDL cells (4)
– Bone cells (3)
 Root Surface Treatment
• Chelating agents like EDTA and citric acid can
expose the collagen fibrils through
demineralization and may improve new
attachment
 Bone Graft Materials
• Autograft= from yourself
• Allograft= from another human, usually cadaver
• Xenograft= from another animal, usually cow
• Alloplast= synthetic or inorganic
• Osteoconductive= scaffold
• Osteoinductive= convert neighboring progenitor
cells into osteoblasts
• Osteogenic= make bone
 Periodontal Surgery Summary
• Additive • Subtractive
– Periodontal – Resective osseous
regeneration surgery
– FGG – Gingivectomy
– CTG – Apically positioned
– Coronally advanced flap
flap
 Tying It All Together!
• 1 and 2-wall defects à resection, recontour bone to
restore positive architecture
• 3 and 4-wall defects à regeneration, better blood
supply and cell source proximity
• Deep narrow 3-wall is ideal for regenerating infrabony
defects
• Hamp Class II (buccal upper or either buccal or lingual
lower) is ideal for regenerating furcation defects
• Miller Class I with thick gingival biotype and wide band
of keratinized tissue is ideal for regenerating recession
defects
Periodontics
 (1) Antibiotics
• Aims to decrease the number of bacteria in
the periodontal pocket
• Should only be used as an adjunct to
mechanical debridement during phase I
• Aggressive and refractory periodontitis
• Bactericidal and bacteriostatic drugs should
not be given at the same time
 Tetracyclines
• Concentrate in GCF
• Doxycyline only requires one dose per day
which may improve patient compliance
 AMX + MTZ
• Amoxicillin (500mg TID) + Metronidazole
(250mg TID) for 14 days
• Duration is more important than dose—the
longer the better
• Avoid alcohol with MTZ
 Local Delivery Antibiotics (LDA)
• When localized recurrent and/or residual PD
≥5mm with inflammation are still present
following conventional therapies
• Arrestin= Minocycline
• Atridox= Doxycycline
• PerioChip= Chlorhexidine gluconate
 (2) Host Modulation Therapy
• Aims to downregulate the destructive aspects
of the host response
• Should only be used as an adjunct to
mechanical debridement during phase I
• Chronic periodontitis
 NSAIDs
• Inhibit prostaglandins
• Long-term use has side effects
 Bisphosphonates
• Inhibit osteoclasts
• BRONJ is a significant side effect
 Subantimicrobial Dose Doxycycline
(SDD)
• Inhibits MMPs (collagenases)
• 20mg twice daily for 3-9 months (Periostat)
• Only one of these that is currently approved
by the FDA and accepted by ADA
 Locally Administered Host-Modifying
Agents
• Emdogain= enamel matrix proteins
• PDGF= GEM 21S
• These surgical adjuncts may also influence
periodontal regeneration
 (3) Occlusal Correction
• Sometimes the root of the problem is
malocclusion
• Traumatic occlusion= injury to the periodontium
resulting from occlusal forces that exceeds the
reparative capacity of the attachment apparatus
 Traumatic Occlusion
• Primary occlusal trauma= caused by excessive
forces on a normal periodontium
• Secondary occlusal trauma= caused by normal
occlusal forces on a reduced periodontium
• Fremitus= vibration of teeth upon closing
 Occlusal Therapy
• Occlusal therapy should be delayed until after
inflammation is resolved
• Occlusal adjustment (coronoplasty)= selective
reshaping of occlusal surfaces
• Interocclusal appliance (bite guard)= redistributes
occlusal forces to minimize excessive force on
individual teeth
 Splinting
• Improve patient comfort and function by
immobilizing excessively mobile teeth
• Not indicated for fremitus or mobility unless it
bothers the patient
 (4) Furcation Correction
• Sometimes a furcation involvement makes
cleaning the involved area near impossible
 Furcation Correction

Furcation Tunneling Root Amputation/ Hemisection/

Plasty Root Resection Premolarization
Periodontics
 Toothbrushing
• Bass method= sulcular brushing where bristles
are placed at gingival margin at a 45 degree angle
to the tooth, the bristles extend about 0.5mm
subgingivally to effectively disrupt plaque buildup
in the cervical area
 Toothbrushing
• Soft nylon bristle brushes do not tend to
traumatize gingival tissues
• Replace brushes every 3 months
 Flossing
• Curve the floss into a C-shape against the side
of the tooth
• Rub the floss gently up and down along the
side of each tooth
• Don’t forget to floss behind your back teeth
 Waterpik
• Home water irrigation systems are designed to
flush out gross food debris and reduce
bacterial load on the gingiva, NOT biofilm on
the tooth surface
 Epidemiology
• Chronic > LAP > GAP > Refractory
• Most prevalent in males of African descent
 Maintenance
• Re-evaluation= 4-8 weeks after phase I non-
surgical therapy
• Periodontal maintenance= every 3 months for
first year