Diseases of the periodontium

DR.AFSHEEN ANWAR DHANANI

PERIODONTIUM

Periodontal tissues include four defined structures:

• gingiva,
• cementum,
• alveolar bone,
• periodontal ligament
Function :
the supporting structure of a tooth, helping to attach the tooth to surrounding
tissues and to allow sensations of touch and pressure
 Epidemiology of periodontal diseases
• The term gingivitis is used to designate inflammatory lesions that are
confined to the marginal gingiva.once the lesions extend to include
destruction of the connective tissue attachment of the tooth and loss of
alveolar bone the disease is designated periodontitis
• chronic inflammatory periodontal disease of varying severity affects
practically all dentate individuals
• gingivitis is common in children even by the age of 3 years and early
periodontitis may be detected in teenagers
• the extent and severity of disease increase with age
• epidemiological data show that whilst the early periodontitis is very
common in adults advanced disease only affects about 10-15 % of the
population
• tooth loss as a result of periodontak destruction is uncommon before the
age of 50 years
 Aetiology of periodontal diseases
Dental plaque is the essential aetiological agent
in chronic periodontal disease:
• strong positive association between dental
plaque and prevalence and severity of
periodontal disease
• not taking care of oral hygiene results in
accumulation of dental plaque and this is
paralleled by onset of gingivitis.plaque
control rapidly restores the tissues to health
 Healthy periodontal tissues

• scanty flora located almost entirely

supragingivally
• microbial accumulation:1-20 cells
• comprises mainly gram positive bacteria
streptococcus and actinomyces species
predominate
 Developing gingivitis
microbial cell layers extend to 100-300 cells in
thickness
actinomyces predominates
proportion of spirochaetes and capnophilic
organisms increases
 established gingivitis
substantial increase in the proportion of obligate
anaerobic gram negative bacteria such as
prophyromonas gingivalis
prevotella intermedia
most of which are located subgingivally
 microbiology of periodontal
disease
• Gram positive cocci decrease as gingivitis
progresses to periodontitis
• Gram negative anaerobic bacilli increase as
disease progresses
• motile forms increase as disease progresses
• periodontal disease involves interaction of
mixtures of the bacteria forming complexes in
plaque
Risk factors for periodontal disease
dental plaque is essential aetiological agent in
the periodontal disease,various local and
systemic factors can modify host’s response to
plaque accumulation and influence the
development and progression of gingivitis and
periodontitis
 local factors
• pre existing anatomy of the tooth,gingiva and
alignment and occlusal relationship
• approximal restorations that may affect the
accumulation and growth of plaque or
interfere with its removal
Systemic diseases and periodontal
diseases
DIABETES MELLITUS:
• Relationship is unclear
• it is commonly held that periodontal disease is more severe
and progresses faster in both type 1 & type 2 diabetes
• vascular changes and defects in cellular defence mechanism
have been suggested as possible ways in which diabetes
could increase suceptibility to periodontal disease
PREGNANCY:
• pre existing gingivitis increases in pregnancy from the second
to the eight month of gestation then decreases
• healthy gingiva are not affected
• hormonal changes modify the tissue response to dental
plaque
• mainly progesterone which affects function and permeability
of gingival microvasculature localized gingival hyperplasia
also occurs during pregnancy (pregnancy epulis)
 NUTRITION
severe and prolonged deficiency of vitamin c
causes scurvy which may be associated with
hemorrhagic gingivitis and edematous
enlargement of the gums
 BLOOD DISEASE
• Acute leukaemia:generalized enlargement of the gingiva due
mainly to infiltration and packing of the tissues by leukemic
cells
• other oral signs of disease can be related to the
pancytopenia and include mucosal pallor gingival
bleeding,gingival ulceration
• severe gingival inflammation,ulceration and advanced bone
destruction may be seen in certain chronic types of
neutropenia such as cyclic neutropenia
 DRUGS
• drugs which affect inflammatory or immune
responses such as immunosuppressants might
be expected to influence the course of
periodontal disease
• phenytoin,(antiepileptic drug) causes gingival
hyperplasia
• immunosuppressants (corticosteroids) equifocal
reduction in disease activity
• calcium channel blockers (verapamil) gingival
hyperplasia
SMOKING
There is considerable body of evidence that
tobacco smoking is an important risk factor for
the development and progression of the
periodontal disease
the mechanism is not fully understood but
smoking impairs phagocytic function of
polymorphoneutrophils and impairs healing
 CHRONIC GINGIVITIS
1. Gingivitis & periodontitis .
▪ Chronic gingivitis
▪ Chronic adult periodontitis.
Less common type of gingivitis
▪ Acute necrotising ulcerative
gingivitis
▪ HIV- associated gingivitis
▪ Herpetic gingivostomatitis
Uncommon type of periodontitis:
▪ Prepubertal periodontitis
▪ Juvenile periodotitis
▪ Rapidly progressive periodontitis
▪ HIV- associated periodontitis
▪ Acute leukaemic periodontal disorder
▪ Miscellaneous periodontal disorder
▪ Gingival hyperplasia
▪ Familial
▪ Drug related
▪ Periodontal abscess
▪ Periodontal atrophy
▪ Pericoronitis
 Disturbance in host-parasite relationship lead to the
development of periodontal disease

microbial plaque Host defences

direct injury salivary factors

toxic products crevicular fluid
enzymes epithelial barrier
antigenic challenge migrating neutrophils
immune response
potential for tissue regeneration and repair
Chronic gingivitis:
▪ Asymptomatic
▪ Red , slightly swollen with oedema
▪ Plaque deposited along gingival margin
▪ In most cases due to local factors (ineffective
tooth brushing)
Factors contributing to
chronic gingivitis
▪ 1) local

▪ Poor tooth brushing technique

▪ Restorations or appliances cause stagnation area
▪ Dental irregularity providing stagnation area
▪ Vit ?? deficiency

▪ 2) systemic

▪ Pregnancy
▪ Down’s syndrome
▪ Poorly controlled diabetes mellitus
Clinical criteria of healthy
of gingiva
▪ Color ……….coral pink
▪ Contour
Free gingiva…………thin and end is knife edge
Attached gingiva…………scalloped
Interdental gingiva……….pointed
▪ surface texture…stippling in attached gingiva & base of
interdental papillae (orange peel appearance)
▪ Consistency………firm & resilient
▪ Depth of gingival sulcus……..0.5 to 2 mm
▪ Type of gingival fluid…….TRANSUDATE
Management
▪ Gentle diagnosis confirmed by resolution of
gingivitis ,when effective oral hygiene measures
become established

▪ Removal local factors

▪ Scaling
▪ Plaque control
▪ Oral hygiene instructions
 1)Pregnancy gingivitis:
▪ Pre existing gingivitis become
more severe in first 2 months
of pregnancy

▪ Inflammatory erythema and

oedema more severe typically

▪ Localized vascular lesions

(pregnancy tumors) may
develop
▪ Pregnancy gingivitis can be abolished by strict
oral hygiene regime
▪ Improve after parturition .

▪ If pregnancy tumor persist ….excision

Down’s syndrome
▪ Gingivitis exacerbated by excessive plaque
formation
▪ As difficulties in establishing effective tooth
brushing habits
▪ It may progress to periodontitis & early tooth
loss
Diabetes mellitus
▪ In poorly controlled diabetes , periodontal
health may deteriorate sharply

▪ Diabetes suffers more severe periodontal

disease
▪ Early tooth loss
▪ Neutrophil defect main factor
 CHRONIC GINGIVITIS
In healthy,non inflamed gingivitis there is continuous migration
of polymorphonuclear neutrophil leukocytes through the
junctional epithelium into the gingival sulcus
the migration of PMN is part of normal host defences to the low
level bacterial challenge to the gingiva which is likely to occur in
healthy mouths. in the absence of adequate oral hygiene the
level of challenge increases as dental plaque accumulates and
gingivitis is initiated
 INITIAL GINGIVITIS
Microscopic area around base of gingival sulcus
acute inflammatory changes
• cellular exudate:enhanced migration of pmn
• fluid exudate:increased crevicular fluid flow
 Early gingivitis
• Lymphocytic infiltration
• impairment of barrier function of junctional
epithelium
• gingival pocket formation
• growth of subgingival plaque
 ESTABLISHED GINGIVITIS
• Expansion of area of inflammation and
destruction of gingival connective tissue
• predominance of plasma cells in
inflammatory infiltrate
• deepening of gingival
pocket,thinning/ulceration of pocket
epithelium
Chronic periodontitis:
▪ Chronic periodontitis AKA chronic adult
periodontitis
▪ Considered to be slowly progressive disease
▪ Mostly observed in adult but can be seen in
children too in response to chronic plaque &
calculus
▪ Defined as infectious disease resulting in
inflammation with in supporting tissues of teeth,
progressive attachment loss & bone loss
 Risk factors
▪ LOCAL FACTOR
▪ SYSTEMIC FACTOR
▪ ENVIRONMENTAL / BEHAVIORAL FACTOR
▪ GENETIC FACTOR
 SIGNS AND SYMPTOMS
▪ Bleeding gum during brushing
▪ Loose teeth
▪ Usually painless
▪ Loss of periodontal attachment…. Pocket formation
▪ Dull,localized pain , radiating pain
▪ Sensitivity to hot/cold
▪ Cratered papilla
▪ gingival bleeding / unpleasant taste
▪ Halitosis
▪ Furcation involvement
▪ Supra/infrabony pockets
▪ SEVERITY: entire dentition or individual tooth

▪ SLIGHT…… 1-2 mm CAL

▪ MODERATE….3-4 mm CAL
▪ SEVERE ………5 mm CAL
▪ local factors are most important in progression of
disease.

▪ Chronic inflammation
▪ Destruction of periodontal ligament fibres
▪ Resorption of alveolar bone.
▪ Epithelial attachment migration towards apex
▪ Pocket formation around teeth
▪ Formation of subgingival plaque & calculus.
 POCKETING
▪ Characteristic features of chronic periodontitis

❑ It is due to slower destruction of gingival soft tissue than periodontal

ligament & bone

❑ Pocket provide protected environment in which bacteria grow freely.

❑ Pocket favors growth of anaerobes …….contributes tissue
destruction
❑ Epithelium is hyperplastic
Periodontal pocket in
periodontitis
Epithelial migration
▪ Epithelial attachment migrates from enamel on
to cementum forming floor of pocket
BONE RESORPTION IN PERIODONTAL DISEASE
▪ proliferation,differentiation and activation of
osteoclasts
▪ in normal remodelling of bone osteoblastic and
osteoclastic activity is tightly coupled
▪ the control of this process involves the activities
of number of cytokines which stimulate or
inhibit either osteoclastic or osteoblastic activity
▪ in pathological process associated with bone
destruction this coupling is distrubed and the
balance is shifted,resulting in bone loss
Role of specific bacteria in
destructive periodontitis
▪ Subgingival plaque ……..gm +ve bacteria
▪ Pocket wall………gm –ve (anaerobes &
spirochaetes
▪ Destructive disease…….porphyromonas
gingivalis,a. actinomycetemcomitans
▪ Extensive bone loss……..prevotella
melaninogenica
 CLINICAL FORMS OF PERIODONTITIS

CHRONIC PERIODONTITIS(adult periodontitis):

• The most common form of chronic periodontal disease and is
characterized by its chronicity
• the onset of the disease is in early adult life but in majority of
the patients does not progress to tooth loss unitll 50 years of
age
• regular pattern of predominantly horizontal bone loss is seen
with suprabony pocketing
• The entire dentition is involved with lower incisors and
molars tending to show the most advanced bone loss
Aggressive periodontitis:
• localized form (juvenile most commonly)
• vertical bone loss
• deep infrabony pockets
• permanent first molars and maxillary incisors teeth are
affected
• number of teeth increases with age
• puberty can be a factor
• generalized form involve entire dentition with rapid bone
loss
periodontitis in systemic disease