PERIODONTOLOGY
MUDr. Hana Poskerová Ph.D.
Dental Clinic St. Anne's Hospital and
Faculty of Medicine Masaryk University
Brno
Periodontitis apicalis Periodontitis marginalis
- result of caries - see below
Do not confuse it, these are two completely different diseases !!!
Periodontium - the tooth
supporting structures
• complex highly specialized
shock-absorbing
pressure senzing system
• consist of four interrelated
tissues supporting the teeth
- covering tissues
- supporting tissues
Periodontal tissue
• Gingiva
• Periodontal
membrane with
periodontal
ligaments (fibers)
• Root cementum
• Alveolar bone
(tooth socket)
Alveolar
bone -
septum
Periodontal
fibers
Cementum
Enamel
Junctional
epitelium
Interdental
papila
Dentin
Sulcus
gingivalis
Papilla
saddle
• GINGIVA
- is one portion of the oral mucosa
- covers limbal part of the alveol
• Free gingiva (a – b)
forms a rim around a tooth neck
• Sulcus gingivalis – gingival fluid
• Dentogingival junction
• Interdental papila – fills the
interdental space
• Attached gingiva (b – c)
firmly attached to the
subgingival structures
• Mucogingival line c
• Alveolar mucous d
a
b
c
d
Healthy gingiva
- white/pink color
- stiff consistency
- stippling
- relativly firm
- no bleeding
Epithelial attachment
Oral epithelium
Connective tissuesupraalveolar
periodontal fibers
Sulcular epithelium
Gingival groove
Sulcus gingivalis
Free gingivaDentin
Enamel
Cementum
Top of
alveolar
septum Infraalveolar
periodontal fibers
A – Gingival fibers
supraalveolar part of
periodontium – supracrestal
attachment
- fix a gingiva to the bone
base, to the tooth root
- provide turgor of gingiva
and its firm adherence to
the tooth surface
- composed from collagen
(that are produced by
fibroblasts)Fibroblast
- narrow groove
sourrounding the tooth
- one wall is made up of
the tooth structure
- the other wall is the
nonkeratinized oral
sulcular epithelium
B,C - junctional epitelium 2mm
A - sulcus gingivalis 0,5-1mm
Sulcus gingivalis
Oral epithelium
Sulcular epithelium
(≈ dentogingival junction,
epithelial attachment)
- surrounds the neck of each
tooth
- conection between soft and
hard tissue, formed by cells
- basal layer and 10-20
suprabasal cell layers
- cells quickly regenerate 4-6
days (oral epithelium 6-12
days)
- undifferentiated,
nonkeratinized epithelium
- attached by
hemidesmosomesB,C - junctional epitelium 1-2mm
A - sulcus gingivalis 0,5-1mm Junctional epitelium
Attached gingiva
Mucogingival line
Free gingiva
Alveolar mucous
membrane
Gingival groove
On the palatal aspect
- the mucogingival line is absent
- gingiva is a part of keratinized mucosa
- rugae palatinae
Width of attached gingiva varies from tooth to tooth and
the width is individual (healthy minimum is 1-2 mm)
Gingival biotype - thick, medium, thin
Thin gingival phenotype, gingival recession at the
tooth 41 - consequence of piercing
Sufficient width of attached gingiva
and thick gingival biotype
There is insufficient width of
the attached gingiva at the
tooth 41 (and 42) and
gingival recession (exposed
neck)
Attached gingiva is
completely absent at lower
canines, there is insufficient
width of the attached
gingiva in lateral incisors association
with gingival
recessions
Shallow vestibulum
(≈ insufficient width of
the attached gingiva)
- pulls the marginal
gingiva
- gingiva is chronically
irritated→ inflammation
- worsens hygienic
condition
- gingival recessions
• Lip frenula attachment
Fyziological
Gingival
Papilllary
Frenulum passing through the papila
• Lip frenula with „high attachment“
- pulls upon the gingival margin and the
interdental papilla
- worsens hygienic condition
- gingiva is chronically iritated and inflammed
- it can cause locallized recession
Frenulum passing
through the papila
Sublingual frenulum breve
Children breast-feeding
and
pronunciation is
more difficult
Adults - gingival
recessions
Periodontal membrane
with periodontal ligaments
B – Periodontal fibers
infraalveolar part connects the
tooth to the alveolar bone
- composed from collagen
(produced by fibroblasts)
- very adaptable and able to
react to the physiological
forces
- high rate of remodeling
and turnover
- Ligaments lead from
lamina dura of an
alveolus to the cement
of a root‘s surface
- Tooth is set in an
alveolus and may move
slightly upon a
mastication load
- Chewing pressure
distributes on the whole
bone socket without
overloading
Periodontal fibers
Plexus gingivalis
- vascular plexus, has rich
blood supply
- enable high metabolismus
of cells and tissue
- hydraulic pressure
distribution of chewing
pressure
- forms a source of
immunocompetent cells to
migrate from this location to
the surrounding tissue
• Root cementum
- covers the root surface
- thickness 0,2 - 1 mm
- avascular
- histologically more
types
• Alveolar bone
tooth socket, interdental septa, interradicular septa
- spongious bone
- compact bone (lamina corticalis)
in the radiograph - linea corticalis - lamina dura
in the region of root apex - lamina cribrosa
Healthy periodontium
- lamina dura is present
- distance cementoenamel junction - margin of
alveolar bone is 1-2 mm
Healthy periodontal tissue
Healthy
gums ?
Etiology of inflammatory perio diseases
– gingivitis, periodontitis
• Exogenous factors
- dental microbial plaque (main factor)
- other local (irritant) factors: calculus and
other plaque retention factors, articulation,
orthoanomalies, soft tissue anomalies…
- smoking
• Endogenous factors (systemic)
- immunity
- systemic diseases (diabetes mellitus, ...)
Calculus - calcified dental plaque
• calculus is always covered by an unmineralized
layer of bacterial plaque
• good place for plaque accumulation
• reservoir and retention web for bacteria and
endotoxins
Calculus - calcified dental plaque
• Calculus is formed by the deposition of calcium
and phosphate salts in bacterial plaque
• salts are present in saliva, in crevicular fluid
Calculus - calcified dental plaque
• inorganic compounds (40% - 80%), as well as
proteins and carbohydrates, microorganisms
• the mineralization starts in centers intracellulary
in bacterial colonies or extracellulary from matrix
with crystallization nuclei (different crystals of
calcium phosphate)
• time required for the formation of calculus is
individually variable
• rate of formation depends on the quality of saliva
and on the level of OH
Origin of minerals and Location
• Supragingival calculus
- source - saliva
- excretion ducts of the
major salivary glands
- on the lingual
surfaces of the
mandibular incisors
- on the buccal
surfaces of maxillary
molars
• Subgingival calculus
- source - sulcular fluid
- on the root surfaces
below the gingival
margin
- can extend deep into
periodontal pockets
• Subgingival calculus
- on the root surfaces below the gingival
margin
- can extend deep into periodontal pockets
Local plaque retention factors
• Locations where there is a
worse approach to teeth
brushing and thus more plaque
accumulation
• Dental calculus (plaque carrier)
• Faulty restorations
- overhanging fillings
- non-fitting crowns
• Orthoanomalies (crowded
teeth…)
• Orthodontic appliances,
dentures
• Anatomical deviations of mucous membranes
- lip frenula with high attachment
- shallow vestibulum, gingival recessions
Local plaque retention factors
DENTAL microbial PLAQUE
- soft deposits (bacterial mass) that form the biofilm
adhering to the tooth and other intraoral surfaces
- may be removed by mechanical means only
DENTAL microbial PLAQUE
• Composed of bacteria in a matrix
• Microorganisms (75 %) a their products
• Matrix (25%)
- bacterial (extracellular polysacharids)
and salivary origin (salivary glycoproteins
and mucopolysacharids)
- calcium, phosphates (mineralization of
plaque)
DENTAL microbial PLAQUE
• Composition and formation rate depends
on
- quality of OH
- quality of saliva
- food, smoking
- immunity
Plaque Formation
• Acquired Pellicle Formation
• Primarily Bacterial
Colonization
• Growth of Plaque
• Maturation of Plaque
1/ Plaque Formation
• Acquired Pellicle Formation
- minutes, 1-2 microns thick
- amorfous film from salivary glycoproteins
- increases the efficiency of bacterial
adhesion
2/ Plaque Formation
• Primarily Bacterial Colonization
- bacterial adhesion by single microorganisms
- extracellular polymeric substances and
fimbriae, enable them to attach rapidly upon
contact
- become established within 24 hours
- G+ aerobs, cocci (Streptococcus sanguis),
G+ rods, G+ fillaments (Actinomyces sp.)
- immature plaque - less adherent
3/ Plaque Formation
• Growth of Plaque in next few days
• bacterial mass increases in quantity due to
adhesion of new bacteria (surface receptors on
G+ cocci and rods allow adherence of G(Fusobacterium
nucleatum) and synthesis of
extracellular polymers
• multiplication of adhering bacteria and growth of
extracellular matrix
• increasing of thickness - diffusion is more difficult poor
diffusion of oxygen - anaerobic conditions
• G- cocci, G+ G- rods and filaments (fusobacteria),
aerobs and anaerobs
4/ Plaque Formation
• Maturation of Plaque
- formation of more complex and mature biofilm
- stable bacterial biofilm
- different morphotypes - cocci, motile rods,
spirochetes (filamentous organisms
predominate)
multiplication of bacteria, new bacterial
species
- mature plaque - very pathogenic
Plaque Formation
• DENTAL microbial PLAQUE
- microbial community
- coexistence of different populations in the
biofilm
- bacteria communicate in different ways
(coagregation, adherence, provid nutrients,
exchange of genetic material)
- this symbiosis gives new features and
greatly increases the resistance of dental
plaque
- can be removed by mechanical means only
• Porphyromonas
gingivalis
• Tannerella
forsythia
• Treponema
denticola
- perio pathogens
Perio patogens
• Aggregatibacter AAC
(Actinobacillus) serotype b
actinomycetemcomitans
• Porphyromonas PG
gingivalis
• Tannerella forsythia TF
• Treponema denticola
• Prevotella intermedia
• Fusobacterium nucleatum
• Peptostreptococus micros
capable of
invading the
soft tissues of
the gingiva
DENTAL microbial PLAQUE
• coronar
• fissural
• supragingival – in gingival region
• subgingival
1 - in sulcus gingivalis of healthy
periodontium
2 - in periodontal pocket
- adherent plaque (enamel, root
surface) composition in gingival
sulcus resembles the
supragingival plaque (G+ and Gcocci,
Actinomyces sp., rods and
filaments), can become
mineralized
- non adherent plaque - freely
moving, G - anaerobs (motile and
nonmotile rods), larger number of
spirochets, no intermicrobial
matrix, important role in the
progression of periodontitis,
bacterial invasion (AAC, PG, TF)
Subgingival plaque (sulcus × pocket)
DENTAL microbial PLAQUE - pathogenity
Supragingival plaque – consequences:
- bacteria in dental plaque produce acids 
caries
- mineralization  supragingival dental
calculus
- increase amount and source of bacterias in
oral cavity
DENTAL microbial PLAQUE – pathogenity
for perio tissue
1 Direct effect
a / bacterial products
- enzymes (proteases,collagenases,hyalouronidases)
- endotoxins (lipopolysaccharides of the bacterial
wall)
- exotoxins (leucotoxin AAC)
- indole, skatol, ammonia, hydrogen sulphide
b / invasion of microorganisms into perio tissue (AAC,
PG, TF)
DENTAL microbial PLAQUE - pathogenity
2 Indirect effect
- via inflammatory mediators (IL –1,6, TNF,
PGE)
- bacterial antigens sensitize cells of the
immune system and activate the immune
response of the host
- there is hypersecretion of inflammatory
mediators (especially by macrophages),
which activate osteoclasts, resulting in bone
resorption
Pathogenity of plaque
• depends on
- amount and composition of plaque
- virulence of microorganisms
- ability to invade tissues (direct invasion true
infection)
• immunity reaction of organism
accumulation of plaque along the gingival
margin leads to inflammatory reaction of
the soft tissue
Host defence reaction
• Acute non-specific host response - first and rapid reaction
- non-specific immune cells (macrophage, neutrophil, or
dendritic cell) function in the first line of defense against
infection or injury
- cells of the innate immune system do not have specific
responses and respond to each foreign invader using the
same mechanism
• Specific (acquired, adaptive) immunity reaction
- this type of immunity creates immunological memory after an
initial response to a specific pathogen
- leads to an enhanced response to subsequent encounters
with that pathogen. This process of acquired immunity is the
basis of vaccination
- includes both humoral immunity components and cellmediated
immunity components
Acute nonspecific host response
• Inflammation - PolyMorphoNuclearLeucocytes chemotaxis,
diapedesis, adherence to bacteria,
phagocytosis, microbicidal activity, complement
system
Specific immunity reaction
• immunological memory after an initial response to a specific
pathogen
• the immune system responds to antigens by producing cells
that directly attack the pathogen, or by producing special
proteins called antibodies
• defense cells recognize antigen
• Lymfocytes
- T cells - cell mediated reaction
- B cells - antibody response upon contact with
antigen; they differentiate into plasma cells
(that produce antibody)
Dental biofilm and systemic diseases
• Inflammation is not only a local matter of the
periodontal tissue, but bacteria and inflammatory
mediators enter the systemic circulation
• Bacteremia
• Inflammatory mediators in systemic circulation
(interleukins, TNF alpha, prostaglandins…)
see http://www.efp.org/newsupdate/oral-health-
and-general-health
Dental biofilm and systemic diseases
• 9th European Workshop in Periodontology “Periodontitis
and Systemic Diseases” 2012
• The Perio-Diabetes Workshop 2017 (organised jointly by the
European Federation of Periodontology (EFP) and the
International Diabetes Federation (IDF)
• See below https://www.efp.org/perioworkshop/workshop-
2012/index.html
Gingivitis - symptoms
• gingival bleeding
• redness to livid colour
• swelling
• gingiva loses its turgor
• tenderness or pain
- inflammation of the gingival
tissue surrounding a tooth
- reversible
Gingivitis showing
edema, redness
and bleeding on
probing
Gingivitis
1. Plaque - Associated Gingivitis (90 - 95%)
• Gingivitis induced - with plaque only
- modified by local factors
• Gingivitis modified by systemic factors
- hormone induced gingivitis (puberty,
pregnancy)
- DM
- medications
- malnutrition (vit C)
1/ Gingivitis induced with plaque only
with plaque only/+ local factors (overhanging fillings, crowns, bridges, mouth
breathing, crowding of teeth, fixed ortho
apliances, soft tissue anomalies,... )
2/ Gingivitis modified by systemic factors
• hormone induced gingivitis - puberty, pregnancy
2/ Gingivitis modified by systemic factors
• diabetes mellitus
3/ Gingivitis modified by medication –
hyperplastic gingivitis
- Calcium channel
blockers (nifedipin)
- Hydantoins
(fenytoin)
- Cyklosporin
4/ Gingivitis modified by nutrition
• Avitaminosis C (scurvy)
Acute necrotizing ulcerative gingivitis
• Painful, rapidly progressive inflammation of gingiva
• Spirochets, fusiform bacterias
• Starts usually without general symptomes
• Gingivitis + crateriform ulcerations of ID papillae,
necrosis at ID papillae
2. Non - Plaque - Associated Gingival
Diseases (5 – 10%)
• Bacterial, Viral or Fungal associated lesions
• Hereditary Gingival Diseases
Gingival fibromatosis
• Gingival Manifestations of Systemic Diseases
Mucocutaneous Diseases (Lichen Planus,
Cicatricial Pemphigoid, Pemphihus)
• Allergic reactions of the gingiva
• Traumatic lesions of the gingiva
2. Non - Plaque - Associated Gingival Diseases
Primary Herpetic
Gingivostomatitis
Desquamative gingivitis
– pemphigus
– pemphigoid
– lichen planus
Overgrowth of gingiva (hyperplastic
gingivitis) in acute leucemia
- there is a multiplication
of leukemic cells in the
gingiva
- gingival ulcerations
2/ Periodontitis
Inflammation of the perio
apparatus of the tooth
- inflammatory destruction
of the junctional
epithelium and gingival
ligaments
- periodontal pocket
formation
- resorption of alveolar
bone
- irreversible
Periodontitis
- inflammation of
gingival tissue extends
into the junctional
epitelium
- attachment damage
- loss of alveolar bone
periodontal pocket
- irreversible
Initial periodontitis
• Symptoms are mild
- gum bleeding after
irritation
- gingival edema
- redness of the gingiva
- probing up to 6 mm
- mild bone resorption
Moderate periodontitis
Advanced periodontitis
- deep periodontal pockets
over 6 mm
- periodontal abscess, pus
between teeth and gums
- tooth mobility, teeth tend to
shift or lose itself
- significant bone resorption
- bad breath
periodontal pocket
bone resorption
periodontal abscess tooth mobility, teeth shifted
gingival recessions
Periodontitis - classification
• Older classification
Chronic periodontitis (adults, slower progression)
Aggressive periodontitis (beginning in younger
age, rapid progression, significant proportion of
AAC)
• New classification (from 2018)
Stage I - IV (depending on attachment loss)
Grades A - C (slow, medium, fast progress)
Chronic periodontitis (90 %)
localized / generalized
Aggressive periodontitis (5-10 %)
localized / generalized
Periodontitis – as a manifestation of systemic
disease associated with genetic disorders
(rare cases)
Periodontitis
Man, 35 years old
Woman, 72 years old
Agressive
periodontitis
- generalized
- IV/C
Chronic
periodontitis
- generalized
- III/A
• Chronic periodontitis
- adults
- polymicrobial infection
- continous and slowly progression
- horizontal resorption
Woman, 70 years old
• Agressive periodontitis
- early onset
- rapid attachment loss and bone destruction
- possible familial aggregation of disease
- except for periodontal disease, patients are
systemically healthy
- tissue destruction is greater than would be
expected given the level of local factors including
bacterial plaque
• Agressive periodontitis
- elevated levels of
Actinobacillus actinomycetemcomitans (AAC)
Porphyromonas gingivalis (PG)
- phagocyte abnormalities and increased production
of prostaglandin E2 and interleukin-1β
Woman, 30 years old
Periodontitis – as a manifestation of
systemic disease
• associated with genetic disorders
• Papillon - Lefevre syndrom
- uncommon inherited autosomal recessive
disease
- hyperkeratosis of the palms and soles (knee,
elbows)
- advanced periodontitis (both deciduous and
permanent dentitions)
- at 20% immunologic defects
12 years old boy
10%
10%
80%
Healthy Agressive advanced periodontitis
Gingivitis + Mild or moderate chronical periodontitis
Prevalence
of perio
diseases
90-95%
Periodontal therapy
• inseparable part of dental therapy
• the goal is to eliminate the etiologic factor
• decrease the level of pathogenic
microorganisms
• eliminate inflammation and periodontal pocket
• Gingivitis ? Type?
• Periodontitis ? Chr - Agr?
• Gingival recessions?
Periodontal therapy
• Preliminary phase
• 1 - Initial phase of periodontal therapy
• Evaluation of response
• 2 - Surgical phase
• Evaluation of response
• 3 - Restorative phase
• Evaluation of response
• 4 - Maintenance phase (supportive therapy,
recall)
1- Initial phase of periodontal therapy
• Plaque control - oral hygiene
(motivating and instructing the patient, control)
• Elimination of plaque retentive areas and Correction of
irritating factors - removing all local irritants that may cause
gingival inflammation)
- reduction of naturaly occuring plaque retentive areas
- removal of iatrogenic irritants
• Supragingival calculus removal
• Subgingival scaling and root planinig
• Antimicrobial therapy
• Temporary restorative treatment and prosthetics (caries, root
canal therapy, occlusal therapy, splinting)
1a - Motivation, education,
oral hygiene instruction
Special tablets or rinses can colour plaque
Oral hygiene products
• Toothbrush
• Single toothbrush
• Dental floss (waxed, unwaxed, tape,
flossholder)
• Interdental cleaners (correct size !)
• Toothpaste (fluorid, antimicrobial agents,
anticalculus agents)
• Oral irrigators
• Mouth rinses
Toothbrush
• short head
• soft, medium, multitufted, straight bristels
Totth brushing techniques
• Fones method – for children
• Charters method
• Stilmann method
• Bass method
Totth brushing techniques
• Charters method
Totth brushing techniques
• Stilmann method
Totth brushing techniques
• Bass method
Pay attention !!!
• Horizontal toothbrushing
• Hard bristels
• Toothbrushing too
frequently
- abrasion of the tooth
structure
- gingival recession (root
exposure, hypersensitivity)
Single toothbrush
„ siwak“
Retention of plaque
• Crowded teeth
• Orthodontic
apliances (braces)
• Implants
Interdental hygiene
• Dental floss • Interdental cleaners
Flossholder
Superfloss
Floss - waxed, unwaxed
Flossing
- break off about 15 - 20 cm
- roll floss around middle fingers
- hold the floss between thumbs and index finger
- guide floss between your teeth- curve it into a C shape against one tooth
- slide it into the space between the gum and the tooth
- move the floss up and down
- do not forget back side of last tooth
Beware of choosing the right
sizes of interdental brushes !!!
Interdental probe
Irrigators
water sprays don‘t
remove plaque !!!
How to clean bridges
How to clean orthodontic appliances
How to clean implants
Toothpaste
• Abrasive - polishing compounds
(improve mechanical cleaning)
• Fluorid compounds (NaF, Aminofluorid)
• Antimicrobial compounds (triclosan, CPC,
CHX)
• Anticalculus compounds
Mouthwash - antiseptic agents
• Chlorhexidin (0.06 – 0.2 %) gold standard
• 0,2% CHX max 2 weeks; 0,12% 0,1% 0,06%
• Unpleasant side effects
- stainig of teeth and tongue
- taste disturbances
- mucosal desquamation
It is not necessary to rinse daily with antiseptic
mouthwash, we use it at some stage of
periodontal treatment
• Adjunct during initial therapy
• Desinfection of oral cavity before dental treatment
• In handicapped patients
• Periodontal surgery
Initial phase
1b - Supragingival - removal of the
calculus and bacteria (hand and
sonic /ultrasonic instruments)
- recontouring defective
restorations and crowns
Scalers – hand instruments
Initial phase
1c - Subgingival treatment of perio pocket scaling
and root planinig (SRP)
- removal of subgingival plaque and callculus
- smoothing of the dental root surface
Gracey curettes – scaling and root planinig
Results of scaling and
root planing
- debridement of bacteria
and calculus
- removal of infected
cementum and dentin
- a shift in the microbial
population
G- → G+
anaerobs → aerobs
spirochets, rods → cocci
Healing after scaling and
root planing – by repar
(scar healing)
- epithelial and connective
tissue
- long junctional epithelium
1d - Antimicrobial prophylaxis
• Local - oral rinse (usually with CHX)
reducing growth of plaque, CHX is not able
to destroy existing plaque !!!
• Systemic antibiotics treatment (against
anaerobes - metronidazol, amoxycilin,
tetracyclin) if needed (aggressive
periodontitis), always at the same time as
treatment of perio pockets (SRP)
2 - Surgical phase
• Elimination of periodontal pockets
• Better gingival configuration
- better conditions for oral hygiene
2a/ Flap surgery in case of
unsuccessful conservative
therapy
- treatment of a defect under
direct visual control
- surgical exposure of the
root by opening gingival
flap
- removal of residual
subgingival plaque and
callculus
- smoothing of the dental
root surface
- open operation field
- the flap is raised and then
fixed
Flap surgery – open flap curettage
2b/ Mucogingival surgery
• Periodontal-prosthetic corrections • Crown lengthening • Socket
preservation • Ridge augmentation • Esthetic surgical corrections •
Coverage of the denuded root surfaces • Reconstruction of papillae
• Esthetic surgical correction around implants •
Upper frenulectomy in connection with ortotreatment of diastema
Enlargement of attached gingiva with epithelial graft from palate
Clean teeth are the main condition
of healthy teeth and periodontium