2. Inflammation is the primary pathological feature of
periodontal disease
Host susceptibility accounts for differences in the
severity of periodontal disease from one individual to
another
Susceptibility to periodontitis influenced by a number
of factors, including systemic diseases and conditions.
Presence of chronic inflammatory periodontal disease
may significantly affect systemic conditions such as
coronary heart disease,
stroke
glycaemic control or
pregnancy outcomes.
3. The relationship between periodontal disease
and systemic health is thus a two-way road,
with systemic host factors acting locally to
reduce resistance to periodontal destruction,
and the local bacterial challenge generating
widespread effects with the potential to induce
adverse systemic outcomes.
4. Certain systemic disorders and conditions alter host
tissues and physiology, which may impair
host barrier integrity and
host defence to periodontal infection, resulting in more
destructive disease.
The interrelationships between periodontal infections
and host defence are complex.
Environmental, physical, and psychosocial factors
have the potential to
alter periodontal tissues and
the host immune response, resulting in more severe
periodontal disease expression.
These disorders and conditions do not initiate
periodontitis, but they may predispose, accelerate, or
5. Endocrine disorders and hormonal changes
Haematological disorders and immune
deficiencies
Stress and psychosomatic disorders
Nutritional influences
Other systemic conditions
7. Reduction in defence mechanisms and
increased susceptibility to infections
Higher prevalence and severity of periodontal
disease in diabetics than in non-diabetic
persons with similar local factors.
Findings include
↑LOA
↑BOP
↑tooth mobility.
8. A, Adult with diabetes (blood
glucose level 400 mg/dl). Note the
gingival inflammation,
spontaneous bleeding, and
oedema.
B, Same patient as in A after 4 days
of insulin therapy (blood glucose
level <100 mg/dl). The clinical
periodontal condition has
improved without local therapy.
C, Adult patient with
uncontrolled diabetes. Note
the enlarged, smooth, red
gingiva with initial
enlargement in the anterior
area.
D, Lingual view of the right
mandibular area in same
patient as in C.
E, Suppurating abscess on the buccal surface of the maxillary
premolars in a patient with uncontrolled diabetes.
9. The Diabetic patient.
A, Gingival inflammation and
periodontal pockets in 34-year-old
patient with diabetes of long
duration.
B, Extensive, generalized bone loss in
the patient shown in A.
12. A, Marginal B, Localized,
gingivitis and easily incipient gingival
bleeding gingiva in a enlargement
woman 5 months between the
pregnant. maxillary central
and lateral
incisors in a
woman 4 months
pregnant.
C, D, Extensive
Generalized gingival
gingival enlargement
enlargement localized on the
of the papilla buccal surfaces of
and gingival lower molars in a
margins on pregnant woman.
the facial
surface of the
maxillary
incisors in a
pregnant
woman.
13. Immuno-suppressive therapy (exogenous
steroids)
May affect bone density and physiology
Widespread effects on the periodontium
Stress- induced (endogenous) cortisol may
produce some effects on periodontium by
diminishing the immune response.
14. Generalized demineralization of the skeleton
Proliferation of the connective tissue in the
enlarged marrow spaces
Formation of bone cysts and giant cell tumours
Oral changes include
malocclusion and tooth mobility,
radiographic evidence of alveolar osteoporosis with
closely meshed trabeculae
widening of the periodontal ligament space
absence of the lamina dura
radiolucent cyst-like spaces
15. Secondary hyperparathyroidism in 35-
year-old woman with advanced kidney
disease. This periapical radiograph shows
ground-glass appearance of bone and loss
of lamina dura. (Courtesy Dr. L. Roy
Eversole, San Francisco.)
16. A, Periapical, and B, occlusal,
radiographic views of brown tumours
in patient with hyperparathyroidism.
(Courtesy Dr. L. Roy Eversole, San
Francisco.)
19. Acute myelocytic
leukaemia.
A, View of patient's face.
Note the elevated, flat
macules and papules
(leukaemia cutis) on the right
cheek.
B, Close-up view of skin
lesions.
C, Intraoral view showing
pronounced gingival
enlargements.
D, Occlusal view of upper
anterior teeth. Note the
marked enlargement in both
the facial and the palatal
aspects. (Courtesy Dr. Spencer
20. A, Anterior view of patient with acute
myelocytic leukemia. Interdental papillae
are necrotic with a highly inflamed and
swollen base.
B, Palatal view demonstrating extensive
necrosis of interdental and palatal tissue.
21. Diffuse pallor of
gingiva in patient with
Smooth tongue in anaemia. The
patient with discoloured, inflamed
pernicious anaemia. gingival margin stands
out in sharp contrast
to the adjacent pale,
attached gingiva.
22. Thrombocytopenic purpura.
A, Hemorrhagic gingivitis in patient with
thrombocytopenic purpura. Spontaneous bleeding from
the gingival sulcus in patient
B, Marked reduction in severity of gingival with thrombocytopenia.
disease after removal of surface debris and careful Normal coagulation is
scaling. evident by the large clot that
forms in the mouth.
However, platelets are
inadequate to establish
haemostasis.
23. Pre-pubertal periodontitis
A, Clinical presentation of 10-year-old male with
cyclic neutropenia and agammaglobulinemia. Note
the severe erythema and migration of teeth caused
by loss of bone support.
B, Panoramic radiograph demonstrating severe bone
loss around all permanent teeth that have erupted
into the oral cavity.
24. Dentition of 17-year-
old boy with
Papillon-Lefèvre
Syndrome. The Severe periodontal
missing teeth were destruction in 14-year-old
exfoliated. patient with Down’s
Syndrome.
25. Documented relationship between stress and
acute necrotizing ulcerative gingivitis (ANUG)
Connection between psychological conditions
such as stress and other forms of periodontal
disease (e.g., chronic periodontitis) has been
difficult to establish.
The types of stress that lead to periodontal
destruction appear to be more chronic or long
term, and less likely to be controllable by the
individual.
26. Psychosocial stress, depression and coping
Stress-induced immuno-suppression
Influence of stress on periodontal therapy
outcomes
Self-inflicted injury
27. Type of stress
Ability and manner of coping of the with stress
Correlate with destructive periodontal disease.
Emotional coping methods appear to render
the host more susceptible to the destructive
effects of periodontal disease than do practical
coping methods.
28. Depression might have a negative effect on
periodontal treatment outcomes
Non-responsive patients generally have a more
passive, dependent personality.
Non-responders often report more stressful life
events in their past.
29. Impact the periodontal health through changes
in the individual's behaviour
Complex interactions among the nervous,
endocrine, and immune systems.
Individuals under stress may
have poorer oral hygiene,
may start or increase clenching and grinding of their
teeth
may smoke more frequently.
Individuals under stress may be less likely to
seek professional care.
30. Neurotic habits, such as
grinding or clenching the teeth,
nibbling on foreign objects (e.g., pencils, pipes),
nail biting,
smoking,
are all potentially injurious to the teeth and the
periodontium.
Self-inflicted gingival injuries have been
described in both children and adults
31. Severe gingival recession of all lower
incisors, which was discovered under
general anaesthesia in an uncooperative,
institutionalized adult with mental
impairment. The patient was known to
pace around the home with all four fingers
inside his lower lip.
32. There are no nutritional deficiencies that by
themselves can cause gingivitis or periodontitis.
Nutritional deficiencies may accentuate the effects
of plaque-induced inflammation in susceptible
individuals.
There are nutritional deficiencies that produce
changes in the oral cavity.
These changes include alterations of tissues of the
lips, oral mucosa, gingiva, and bone.
These alterations are considered to be periodontal
and oral manifestations of nutritional disease.
34. Rare familial skeletal disease characterized by
rickets, poor cranial bone formation,
craniostenosis, and
Premature loss of primary teeth, particularly
the incisors and reduced cementum formation.
In patients with minimal bone abnormalities,
premature loss of deciduous teeth may be the
only symptom.
In adolescents, this disease resembles localized
"juvenile" (aggressive) periodontitis.
36. Extensive marginal Characteristic clubbing of the
inflammation with ulcero- fingers in adolescent patient
necrotic lesions and with Tetralogy of Fallot,
periodontal destruction consistent with untreated
congenital cyanotic heart
disease.
The apparent increase in dental disease may be attributed to poor oral hygiene
and a general lack of dental care rather than a disease-related aetiology.
37. The ingestion of metals such as
Mercury,
Lead, and
Bismuth
in medicinal compounds and through
industrial contact may result in oral
manifestations caused by either intoxication
or absorption without evidence of toxicity.
38. A, Linear discoloration of the
gingival in relation to local
irritation in a patient receiving
bismuth therapy.
B, Biopsy specimen showing
bismuth particles engulfed by
monocytes/macrophages.
