Periodont

al
Disease-2
HARSHIT BANSAL
BDS 2nd YEAR
 Gingival Enlargement
associated with SYSTEMIC
FACTORS
Classification of Periodontitis

The Periodontal Pocket

Aggressive Periodontitis

Necrotizing Ulcerative
Periodontitis
L

Periodontal Lateral Periodontal Abscess

Disease PERI-IMPLANTITIS
GINGIVAL ENLARGMENT WITH
SYSTEMIC FACTORS

Conditioned Enlargment
Due to systemic condition of patient
Bacterial plaque essential for initiation
three types

 HORMONAL

NUTRITIONAL
ALLERGIC
HORMONAL ENLARGMENT
 Direct or indirect association with endocrine
imbalance
 Often occur in puberty
 Reasons- hormonal imbalance
- poor oral care
- irritation due to tooth eruption
- poor nutrition
 During pregnancy- gingivitis in pregnancy
increased level of estrogen and progesterone-vascular
permeability > -gingival edema inflammatory response
 NUTRITIONAL
ENLARGEMENT
 Vitamin “C” Deficiency- spongy bleeding
gums of scurvy classically includes gingival
enlargment

 Vitamin deficiency + inflammation produce

enlargment
 Gingiva become tender ,swollen ,and
edematous. bleed upon slight provocation

 Sometimes ulceration and necrosis of papillae

also occur
 ALLERGIC ENLARGEMENT
 PLASMA CELL GINGIVITIS -(atypical gingivitis )
-hypersensitive reaction to component of
.chewing gum
.dentifrices
. Some dietary component

 Clinical features- young women, soreness of mouth,

mild marginal gingival enlargement extends to
attached gingiva appears swollen erythematous
with loss of stippling
 Tongue and lips involved appears dry and
exhibit cracks or fissures
 Histological features –surface epithelium
hyperplastic ,intercellular edema ,
 Infiltration of connective tissue by chronic
inflammatoy cells
 Vascular dilatation
 Treatment –allergen should be removed ,study
patient history
 Topical and systemic steroids given
 PERIODONTITIS
 INRODUCTION-
Periodontitis is defined as an inflammatory disease
of the supporting tissue of the teeth caused by
specific microorganisms, resulting in progressive
destruction of the periodontal ligament and
alveolar bone with pocket formation, recession, or
both.
 Classification

 CHRONIC

 AGGRESSIVE

 MANIFESTATION OF SYSTEMIC
DISORDERS
 ACUTE PERIODONTITIS DUE TO
OCCLUSAL TRAUMA
 CHRONIC PERIODONTITIS
(PYORRHEA,PERIODONTOCLASIA)
 MOST COMMON
 Begin as marginal gingivitis
 More in adult ;
 ETIOLOGY-same as for gingivitis but for longer
duration .local factors such as plaque, calculus, food
impaction and irritating marginal fillings are
common.
 Associated with actinobacillus
actinomycetemcomitans,porphromonas gingivalis
and prevotella intermedia;
INCIDENCE-

 Rarely seen before 18 but rapidly increases

after 45
 Bone loss is more in men
 Pocket formation increases with age;
 Immunological features-both cellular and
humoral immunity are implicated in
destruction of periodontal tissues.
 Without exception immunodeficient patient
show less gingival inflammation than
immunocompetent
 This is because immunoglobulins have minimal
effect on
microbes in dental plaque.

 Cystatin c is found in periodontitis fluids this is a

inhibitor of lysosomal proteinases

 So it is seen cystatin c level increases with

progression of disease
 CLINICAL
FEATURES-
 Supra and subgingival plaque accumulation (frequently
associated with calculus)
 Gingival inflammation
 Pocket formation
 Loss of periodontal attachment
 Occasional suppuration
 Poor oral hygiene –
 gingiva is typically may be slightly to moderately swollen
 Color- pale red to magenta
 Surface topography – loss of stippling
 Blunted or rolled gingival margin
 Flattened or cratered papillae.
 Furcation
 Tooth mobility
SYMPTOMS-
 Bleeding gums during brushing or eating
 Increasing spacing between their teeth
 Loose teeth
 Usually painless, but sometimes localized dull
pain radiating deep into the jaw
 Sensitivity due to exposed roots
 Food impaction
 Halitosis
 Gingival tenderness or itching
Marginal periodontitis is also subclassified on the
basis of severity and degree of tissue destruction

2-3 mm 3-5 mm .>5 mm

 TRAUMA FROM OCCLUSION

Clinical features:
•Increased tooth mobility
•Widening of the periodontal space, particularly in the gingival region of
the root (angular destruction of bone.

•These changes are adaptation

phenomena to the increased
function. It does NOT produce
gingival inflammation or the
formation of periodontal pockets
 The Periodontal Pocket

 A periodontal pocket is a pathologically

deepened sulcus: it is one of the
important clinical features of periodontal
disease
 Clinical Signs:
 Enlarged, bluish red
marginal gingiva with
a “rolled” edge separated
from the tooth surface
 A break in the faciolingual

continuity of the
interdental gingiva
 Shiny, discolored, and puffy gingiva

associated with exposed root surfaces

 Gingival bleeding

 Looseness, extrusion, and migration of

teeth.
 SYMPTOMS:
1. Localized pain or a sensation of pressure after
eating, which gradually diminishes
2. A foul taste in localized areas.
3. A tendency to suck material from the
interproximal spaces.
4. Radiating pain “deep in the bone”
5. A “gnawing” feeling or feeling of itchiness in the
gums.
6. Sensitivity to heat and cold; toothache in the
absence of caries.
7. Complaints that food sticks between teeth or
that the teeth feel loose or a preference to eat
on the other side.
 Types of Periodontal Pockets
GINGIVAL PERIODONTAL
POCKET POCKET

 Relative or false  Absolute or true pocket

pocket
 Occurs with destruction
 formed by gingival of supporting periodontal
enlargement tissues
without destruction
of the underlying  Has two types:
periodontal tissues. 1. Suprabony – bottom
of the pocket is
 The sulcus is coronal to the
deepened because underlying alveolar
of increased bulk of bone
 The Periodontal Abscess

 A periodontal abscess (lateral or parietal

abscess) is a localized purulent
inflammation in the periodontal tissues.

 CLASSIFICATION ACCDG. TO LOCATION:

1. Abscess in the supporting periodontal tissue
along the lateral aspect of the root
2. Abscess in the soft tissue wall of a deep
periodontal pocket
3. if the abscess balloon the overlying tissue
known as gum boil or parulis
AGGRESSIVE PERIODONTITIS
 Aggressive periodontitis
(AgP) comprises a group
of rare, often severe,
rapidly progressive
forms of periodontitis
often characterized by
an early age of clinical
manifestation and a
distinctive tendency for
cases to aggregate in
families
GENERALIZED AGGRESSIVE PERIODONTITIS
 LOCALIZED AGGRESSIVE
PERIODONTITIS
 Clinically, it is characterized as having
"localized first molar/incisor presentation with
interproximal attachment loss on at least two
permanent teeth, one of which is a first molar,
and involving no more than two teeth other
than first molars and incisors
 Clinical features
1. Age of onset at about puberty.
2. Affects both the sexes
3. Main characteristic
feature  affects mainly the
FIRST MOLARS and INCISORS
4. Lack of clinical inflammation
despite the presence of
deep periodontal pockets.
5. Plaque that is present forms
thin biofilm on the teeth.
6. Plaque contains elevated
levels of :
Aggregatibacter
actinomycetem-comitans

Porphyromonas gingivalis
(in some pts)
7. Disease progresses rapidly and Plaque that is
present forms a thin biofilm on the teeth and
rarely mineralizes to form calculus
8. The rate of bone loss is 3 to 4 times
faster than in chronic
periodontitis.
.
 Radiographic finding:

o Classic diagnostic sign  VERTICAL LOSS of alveolar

bone around the first molars and incisors.
o Other finding  “Arc-shaped” loss of alveolar bone
extending from the distal surface of 2nd premolar to
the mesial surface of the 2nd molar.
o Bone defects are usually wider than usually seen with
chronic periodontitis
 Generalized aggressive
periodontitis
 “Characterized by generalized interproximal
attachment loss affecting at least three
permanent teeth other than first molars and
incisors
 FEATURES
 Usually affecting persons under 30 years of age,
but patients may be older.
 Poor serum antibody response to infecting
agents.
 Generalized interproximal attachment loss
affecting at least three permanent teeth other
than first molars and incisors.
 Pronounced episodic nature of the destruction of
attachment and alveolar bone.
 Localized aggressive Generalized aggressive
periodontitis (LAP) periodontitis (GAP)
AGE OF ONSET Circumpubertal Under 30 yrs of age but older
patients may be affected

DISTRIBUTION Localized 1st molar or incisor Generalized interproximal

presentation with attachment loss affecting at
interproximal attachment loss least three permanent teeth
& not involving more than 2 other than 1st molars & incisors
permanent teeth
SEVERITY Rapid & severe loss of Episodic in nature
alveolar bone
AETIOLOGY Predominantly Aa Predominantly P. gingivalis
IMMUNOLOGICA Robust serum antibody Poor serum antibody response
L RESPONSE response to infecting agent to infecting agent
PRESENCE OF There is minimal amount of There is marked plaque &
LOCAL FACTORS local factors present on the calculus accumulation
affected teeth
FAMILIAL Strong association Unclear association
PATTERN
 Localized Aggressive Generalized Aggressive
Periodontitis Periodontitis

GINGIVAL Lack of clinical Clinical signs of gingival

INFLAMMATION inflammation despite the inflammation are evident
presence of deep pockets
and advanced bone loss

RADIOGRAPHIC Vertical or arc-shaped bone There is generalized

APPEARANCE loss around 1st molars and extensive destruction or
incisors bone loss around involved
teeth
NECROTIZING ULCERATIVE PERIODONTITIS
 Young patients
 Along with nug

 Fever malaise and

lymphadenopathy
 Loss of bone and attachment
 Immune dysfunction play major role
 May occur in hiv +ve patients-cause ulceration
and necrosis of gingiva with pain and
spontaneous
 Seen 73% pt die in 24 months after detection of
nup in hiv +ve pt
 PERI-IMPLANTITIS
 Inflammation of soft tissues
surrounding osseo integrated
implant in function and
progressive bone loss is
termed as peri-implantitis
 Multifactorial process,

may lead to implant

faliure and loss
 Etiology- associated with high degree of plaque
accumulation.
 Smoking and microbial plaque
 Gram –ve anaerobes ,spirochetes ,fusiform bacteria
in high proportions
 Bacterial infection and
biomechanical factors in
relation to extra load on
implant crestal bone loss
 Other factors- status of tissue,
implant design, degree of roughness, poor alignment
of implant ,excessive mechanical load , and oral
hygiene
 Soft tissue response to plaque in mucosa at site of
implant is similar to that seen in gingiva around
teeth
 Lession expand more with time in this and also more

tissue destruction seen compared to gingival lession

 Key virulence factors for destruction –ENDOTOXIN

 Toxin activated macrophage proteases

degrade collagen and proteoglycans

 Macrophages produce cytokines,IL-1,and PG

E2 which activate
osteoclasts  bone resorption
 AILING-implant show symptom of infection but
not yet mobile  display bone loss and pocketing

 FAILING- similar features but is refractory to the

therapy and become worse failed implant is one
that is fractured ,no response to treatment ,mobile
and circumferential peri-implant radiolucency

 Failed implant due To

infection shows-pain,
bleeding on probing,
suppuration, attachment loss
and granulomatous tissue on removal
 Peri-implant mucositis
 Peri-implant mucositis- prolifiration of gingival
tissues and inflammation as redness
 No bone loss
 Peri-implanitis cont…..
 Lession is poorly encapsulated ,
extend into bone tissue
and lead to bone loss
 Associated with
opportunistic pathogens
actinobacillus
actinomycetemcomitans,
porphyromonas gingivalis etc
 This emphasizes on importance of establishing
healthy periodontal condition before implant
placement and regular maintance program thereafter
 Management- systemic antibiotics
with removal of bioflim from implant
 Local therapies-mechanical brushing ,
chemcal like citric acid , chlorhexidine ,
delmopinol effective in cleaning titanium
surface
THANK
YOU..!!!...