Periodontics

Acute periodontal conditions

Pocket activity, and the frequency of the active episodes are of more importance than the
absolute pocket depth especially in regard to treatment planning and prognosis.
Acute pain
Tooth pain Periodontal pain Other
Reversible Periodontal abscess TMJ
Irreversible pulpitis Pericoronitis Trauma
Periapical abscess Endo/perio lesion Oral pathologies
Cracked tooth ANUG
Root fracture ANUP
Occlusion Ulcerations
Dentinal sensitivity Oral pathologies associated with
the gingiva

Classification
1. Gingival/ periodontal abscess: develops during an acute exacerbation of necrotic
tissue.
This is as symptom of severe advanced periodontitis, where tooth mobility is often
associated. Isolated deep pockets, increased amounts of suppuration in the pocket may
lead to the surrounding destruction of the periodontal tissues. From a microbiological
perspective there is also a shift in the composition of the microflora. This may occur:
 Acute exacerbation of existing untreated periodontitis
 During therapy; this may seem strange, however may be related to dislodgment
of calculus fragments.
 Refractory periodontitis
 Also treatment with systemic antibiotics without subgingival scaling. The change
in the microbiota may lead to a super infection. Will usually form multiple
abscesses.
 Frequently found in furcation involvements, and patients with uncontrolled
diabetes (the associated biological effects are, impaired cellular immunity,
decrease in leukocyte chemotaxis/ phagocytosis and bactericidal activity.
Note that periodontal abscess can also occur in the absence of periodontitis: that is there
is impaction of a foreign body i.e. broken toothpick
Diagnosis:
Ovoid elevation
Gingiva is oedematous/red/smooth shiny surface
Pus may be expressed (fistula) or when gently pressed extrude pus from the
pockets
Pain and swelling, described by the patient as a feeling of pressure on the gums
Increased tooth mobility, TTP,
Systemic symptoms can also be involved.
Dramatic widening of PDL and loss of surrounding bone
Differential: Endo abscess, crack, root fracture.
Treatment:
1. Emergency Tx: Give LA, drain the sinus, debride the area, and irrigate with saline
(flush i.e. CHx)
2. Periodontal access, remove calculus, dental anomalies, granulation tissue
3. Only give antibiotics if there is a systemic involvement of lymph nodes.
Metronidazole 400mg.
 2. Pericoronitis:
Is an inflamed operculum of the partially erupted teeth, very common presentation of
wisdom teeth, and therefore more likely to occur in the age group of the 18-30 years.
Important to explain to the patient the pain arises from the inflamed soft tissue and not
the actual tooth itself.
Assoc. symptoms: Odor, bad taste, pain, localized swelling, and pus discharge. Also there
are a few major symptoms (note that these are not uncommon due to the anatomical
location of the wisdom teeth). Difficulty swallowing, limited opening, enlarged lymph
nodes, fever and facial cellulitis.
Treatment:
Initial phase; debride the area under the operculum, irrigate using a monojet
syringe with CHx and saline. Place the patient on CHx mouthwash for a week and
discuss the importance of keeping the gingival tissues in this area clean. Also
note that if there are major systemic symptoms than adjunctive antibiotics
(amoxicillin or penicillin V) in combination with metronidazole are given for one
week.
Definitive treatment: If this is a reoccurring problem, and or the wisdom tooth is
impacted, consider: extraction, operculectomy, or wait and monitor.

3.Acute necrotizing ulcerative gingivitis (ANUG)

This is a “rapid, destructive, non-communicable gingival infection of complex etiology.”

Bacteria: Local factors: Sytemic factors:

poor oral hygiene, plaque
the specific bacteria is retention (overhangs), emotional stress, poor
unknown, however non- crowded teeth, and cigarette nutrition, hormonal
periodontal imbalance, diseases
pathogenshave been smoking.
affecting the immune system
associated. E.g. streps and
staph

ANU
G
The clinical features include:
 Necrosis of the crest of the marginal gingiva: interdental papilla “punched out”
 Rapid destruction of gingival tissues
 Spontaneous bleeding
 Halitosis, and bad taste “metal taste”
 Pain
 Papilla is usually covered in greyish yellow pseudomembrane
 In severe cases there may systemic symptoms (fever, malaise,
lymphadenopathy)
Differential diagnosis: Not to be confused with other rare oral mucosal lesions- acute
herpetic gingivostomatitis, desquamative gingivitis, HIV-related periodontitis,
streptococcal gingivostomatitis, advanced marginal gingivitis, apthous stomatitis, acute
leukemia and dermatoses
Treatment: debriment under LA, irrigate area with betadine, CHx mouth rinse twice daily
for a week, and investigate the causative factor (most important)
4. Acute Necrotizing Ulcerative Periodontitis (ANUP)
Is an infection and necrosis of the gingiva, PDL and the bone, which induces severe pain.
Necrosis and ulceration at the interdental papilla result in deep interproximal crater like
defects, which may cause sequestration of pieces of bone. Upon removal of this bone
there may be evidence of buccal and lingual involvement.
Note that these lesions are most commonly observed in people with systemic diseases,
HIV, immunosuppression, and severe malnutrition.
Treatment: Referred for specialist care, debriment and high doses of antibiotics. Failure
to act quickly will result is rapid bone loss.
Endo/Perio:
5. Perio/Endo lesion Endodontic abscess may drain
Periodontal disease only causes pulpitis when the through the sulcus (path of least
infection has spread to the apex of the tooth, and gains resistance) and form a localized
access to the pulp via the apical foramina. The only other pocket. Once the endodontic
exception is if there is a large lateral canal, which may act therapy is complete, there is
as an entry point. natural healing of the apical bone.
Prognosis: poor, if treatment is commenced, pulp This is the only situation in
extirpation must be carried out before periodontal periodontitis where bone
planning. If only one root is involved, root resection is also reformation may occur.
a viable option.

Surgery in Periodontal disease Rationale and Types

Treatment modalities; closed therapy- scale and clean, and open therapy-surgery or
combination.

Non-surgical intervention
Is the removal of plaque and calculus, with minimal trauma to existing tooth structure.
Depends on accurate determination of correct time intervals between supportive
periodontal therapy, and motivation of patients to maintain oral hygiene- tailored to each
individual. Instruments include: hand scalars, curettes, ultrasonic, OH devices and
mouthwashes and antiseptics.
Advantages Disadvantages
Hand Better tactile sensation in Decreased efficiency in inexperienced
Scalers experienced clinicians clinicians which can cause tooth damage
Ultrasonic Ease of use, even in inexperienced Decreased sensitivity, can cause damage to
Scalers clinicians, cellular disruption, tooth structure, patient discomfort.
access to difficult areas.
Therapeutic effects: Reduction of clinical inflammation, microbial shifts to less pathogenic
microflora, decreased probing depth, gain of clinical attachment, and decrease in disease
progression.

Pathogenesis of healing:
Immediately following non-surgical cleaning, both the pocket epithelium and the junctional
epithelium and part of the lateral connective tissue (adjacent to the dentogingival epithelium) are
removed “curettage” –blunt end removal. Note that NEW epithelial attachment forms NOT repair
of the old epithelium. Long junctional epithelium (healing epithelium) proliferation form the
gingival margin and form surviving strands of epithelium form over the connective tissue wound
surface. Also on the surface of necrotic zone, a layer of leukocytes accumulate, these protect
against bacteria and also mediated healing event (some).
Events summarized:
 8-24 hours: mediators of inflammation are
released, cell proliferation of connective tissue and Detection of residual calculus:
epithelium, and blood clot disintegration. The success of your treatment is
 7 days: Most connective tissue is covered by only as good as your calculus
epithelium, and new attachment is formed against detection, particularly in
the tooth surface, in uncovered areas leukocytes susceptible patients. However the
constitute the barrier towards the environment of literature shows that detection of
the subgingival space. subgingival calculus is low:
 3 months: maturation and remodeling of the tissue, Sherman (1990) showed 77.4%
should not be probed before then, otherwise the with microscopic calculus were
tissue may break down. Note that this does not mean clinically scored are “calculus
that new connective tissue has formed but is a free” and 11.8% of surfaces
reflection of increased tonus of the gingival tissues microscopically free of calculus
preventing the apical placement of the probe. were clinically determined as
“having calculus”
Therapeutic benefit: 1-2 mm attachment in PD. Probing
depth may show decrease of up to 2-4 mm. Must maintain oral hygiene.

Periodontal Surgery
Only considered in conjunction with closed therapy, i.e. subgingival root debriment
(SRD) with and without direct vision.
Outcomes: regenerate PDL/Cementoblast cells.
1. SRD with direct vision: root surface is exposed, (mucoperiosteal flaps, or gingivectomy).
This includes depression, irregularities, anomalies and furcation are all debrided and there is
complete removal of endotoxin containing cementum and smoothed root surface.
2. Reduction and elimination of plaque retentive areas: POCKETS! And additional niches
(furcation, poor margins etc.). These include flap procedures and odontoplasty for furcation
thereby rendered accessible for OH, or root resection.
3. Elimination of inflammations and pocket activity: signs of pocket activity-exudates,
hemorrhage or suppuration. Halt progression of disease and promote tissue shrinkage
(exposure of cervical areas)
4. Enhancing regeneration of periodontal tissue: related to guided tissue regeneration
(early stages only) make it possible to avoid respective surgery.
5. Creation of physiologic morphology:
recreating the contour of marginal periodontium,
enhance the width of attached gingiva (or
unphysiologic frenum attachments).
Types

Periodontal Resective surgery

surgery gingivectomy
Modified widman

Resective
surgery;
Mucogingival Guided tissue
Access For

Surgery regeneration GTR Flap

surgery
pocket depth reduction, and removal of hyperplastic tissue (idiopathic or induced by
medication)
 Gingivectomy: removal of pocket epithelium, connective tissue and mucosal
epithelium. Specifically for horizontal bone loss, (with adequate width of
keratinized mucosa) and gingival hyperplasia. Contraindicated- infra-bony
defects, and aesthetic areas. Post op, sites can be scale/cleaned and probed 2-3
weeks.
 Modified Widman flap: same as gingivectomy except indicated in aesthetic areas,
contraindicated if there is inadequate keratinized mucosa. Post op, no probing or
scale and clean 3-6 months.

Guided tissue regeneration:

GTR placement of a physical/biological barrier to ensure that the root surface becomes
repopulated with PDL and bone cells.
 Epithelial cell: hours to days
 Gingival Connective tissue: days to weeks
 PDL cells: days to weeks
 Bone cells: weeks to months
Post op: Sites that have undergone GTR cannot be probed for a minimum of 6 months,
then length of time is greatly dependent on the material used. I.e. Perioglas (6-12
months) >Bis-Oss (12-18 months)>Emdogain (2-3 years)

Mucogingival Surgery
Corrects soft and hard tissue defects, using soft tissue positioning or grafting. For example
gingival recession, if there is increase in recession, hypersensitivity and aesthetic concerns. –
Lateral sliding flap. Most of the recession defects stay the same but never get better, post
operatively don not probe for 3 months and be gentle.

Surgery in Periodontal disease-GTR and GBR

Therapeutic benefits include: Shrinkage of pocket during resolution of gingivitis, new
collagen formation in the gingiva, long junctional epithelium and periodontal
regeneration.
The Key to periodontal regeneration is the formation of new cementum and bone. The
concept of true regeneration where there is new attachment- new collagen fibres, which
are embedded, in the newly formed cementum. In theory the stem/progenitor cells
populate the bony defect and differentiate into cells forming cementum, bone and
ligament.
Anatomy of the bony defects: Can be either
a) Supra-bony: pockets are formed when bone loss occurs in a horizontal
pattern
b) Infra-bony: pockets occur when bone loss occurs in a vertical/angular
direction
 Furcation involvement: Periodontal bone loss in the furcation can be classified as
Class I: 3mm probing
Class II: > 3mm
Class III: can be probed completely through
Bone Volume: Refers to the amount of bone there is in different areas, i.e. mesio-distal
width and bucco-lingual width. Needs to be considered when planning regenerative
procedures.

Defecet size
Defect Technical
and Predictability
cause difficulties
topography
The three types of materials commonly used in GTR they include: Bone grafts,
membranes, and growth factors.
1. Bone grafts:
a. Autogenous i.e. harvested from patient,
b. Autologous; harvested from the same species
c. Alloplastic: Bioactive glasses eg. Perioglas
d. Xenografts: Bis-Oss (bovine bone) –This is the one used at the hospital.
2. Membranes
a. Xenograft: Porcine – Bioguide
b. Synthetic: Polylactic i.e. Vicryl
3. Growth Factors
a. Xenograft: Enamel matrix protein- Emdogain
b. Autogenous: Platelet rich plasma, rich in PDGF
c. Synthetic
Changes in PD/PAL
-Perioglas:2mm decrease in PD and 2mm gain. There is no or little cementum, mostly LJE
and some connective tissue attachment. Healing time 3-6 months for graft to resorb, and
can continue to improve up to 1 year.
-Bio-Oss/Bio-Gide: 4mm decrease of PD and 3-4mm gain of attachment. Cementum,
connective tissue attachment and bone, has formed LJE. Healing time is 12-18 months
graft to reabsorb, can improve up to 2 years.
-Emdogain: 4mm decrease in PD and 3-4 mm gain in attachment. There is generally
cementum; connective tisse attachment and bone will form LJE. Healing can occur and
continue up to 2-3 years.

GBR –guided Bone regeneration

Involves the placement of physical/biological barrier that promotes the deficient hard
tissue are to become repopulated with bone.
Osteoinduction: Recruitment of immature cells stimulated to develop pre-osteoblast
Osteoconduction: Promotion of bone matrix growth on surface or pores.
Alveolar bone defects:
1. Class I: bucco-lingual deficiency of width
2. Class II: vertical deficiency
3. Class II combination
Materials used:
1. Membranes:
a. Non-resorbable: reinforced/non- Prevalence of recession:
reinforced 1-19% children >1 site
b. Resorbable 50% aged 18-64 >1 site
2. Grafts 88% age >65 have >1 sites
 a. autogenous bone
b. allografts (DFDBA)
c. Xenografts: Bis-Oss
Membranes are also used for GBR, note grafts are used in conjunction with non-reinforced
membranes

Periodontal Aesthetic surgery

Recession: Localized/generalized
Classification of recession
One of the most important things to consider is the
Class I: facial recession classical
gingival biotype of the patient: these are described
Class II: extending beyond the
by Oission and Lindhe (1991). Indicators as
mucogingival fold
mentioned above.
Class III
 Type 1: Thick and flattened
Class IV
 Type 2: Thin and scalloped
Correction
Mucogingival surgery
1. Pedicle grafts:
a. Rotational: lateral sliding flaps, double papilla flap, oblique rotated flap
b. Advanced: coronally repositioned flap, semilunar coronally repositioned flap
2. Free soft tissue grafts
a. Free gingival graft
b. Subepithelial connective tissue graft
Frenectomy

Crown lengthening: to create greater height of the tooth structure in order to properly
restore prosthetically. Note that tooth extrusion orthodontically is also another option
Indications Consideration Contraindication
-Excessive gingival display -Periodontal status and prognosis -Teeth with excessive
-Severe wear, secondary to of the tooth long term periodontal
bruxism -Root anatomy and level of involvement
-Inadequate amount of tooth alveolar crest -Risk of severe
structure -Gingval thickness or radicular furcation
-Subgingival location of fracture bone, probing sulcus, -Extensive caries in the
lines -Esthetics, value endodontic status furcation areas
 -Subgingival location of caries -Apical extent of fractures/caries -Apical extent of
-Facilitate impression taking -Crown-root ratio fracture/caries >4-5
-Location of furcation mm

Soft tissue resection- is indicated when the bone levels are at the correct height to ensure
biological with is accommodated

Supportive Periodontal Therapy (SPT)

Nonspecific plaque and modifying factorsgingivitis, while perio is inflammatory
response to mainly gram negative anaerobic bacteria and
supporting structures.
Treatment goals:
- Control infection
-Remove predisposing factors
-Regulate modifying factors
- -Regenerate to original form
and function
- Maintain lifespan, esthetics

Why SPT?
Irregular SPT are 3-5 times more likely to experiences tooth loss. These appointments
consist of examination and re-evaluation, motivation and instruction (education),
treatment and re-treatment of infected areas (hence highlighting the importance of
thorough noting), polish and apply fluoride.
Also note there are other pre-disposing factors and these include: Enamel projections,
enamel pearl, grooves and fissures on the root surfaces, carious lesions, and resorptive
defects, overhangs, vertical root fractures, and endodontic considerations.
 Patient factors: Age, smoking,
medication, stress, medical
conditions, motivation and
compliance, inital diagnosis
(Aggressive/advanced perio)

Oral Factors: Oral

hygiene, parafunctional
habits, previous history
of tooth loss, bone loss
Tooth factors:
Calculus, probing Diagnosis and age, gingival biotye,
prosthesis
depths, recession and
attachemetn loss, and re-
frucation, bone loss
and suppration and
mobility.
evaluation

The periodontal Risk assessment:

This system