Transcript File

ROLE OF SYSTEMIC DISEASE
IN ETIOLOGY OF
PERIODONTAL DISEASE
It is a well established fact that the primary etiological agent in
periodontal disease is bacterial plaque. The toxins and
enzymes produced by the bacterial plaque elicit inflammatory
and immunologic changes in the periodontal tissues at both
cellular and molecular levels.

These responses can be affected by a variety of systemic
factors that can alter the response of the tissue to plaque.

Certain systemic disorders can have a direct effect on the
periodontal tissues and these represent the periodontal
manifestations of systemic diseases.
Dietary and Nutritional Aspects of
Periodontal Disease



The majority of opinions and research
findings point to the following
Nutritional deficiencies produce changes in
the oral cavity
These are no nutritional deficiencies that by
them selves cause gingivitis or periodontal
pockets.
The consistency of Diet



From the view point of promoting and maintaining gingival and
periodontal health DIET is often stated that a firm and fibrous diet
is more beneficial than an intake of soft and more loosely
textured food.
Diets that are predominantly fibrous are considered
advantageous as they posses the ability to impart a natural
cleansing action to the teeth and the periodontium.
A coarse diet requires vigorous mastication and the plaque that
forms approximately tends to be towards the cleansable buccal
and lingual surfaces of the teeth. However coarse and granular
diets can predispose to a direct traumatic injury to the supporting
tissues
Protein Deficiency and
Periodontal Disease


Proteins are constituents of the organic
matrices of all the dental tissues including the
alveolar bone. The integrity of to periodontal
ligament is also depend upon proteins (amino
acid).
Deprivation of proteins, extreme pathologic
changes or and there is marked degeneration
of periodontal support.
Vitamins and Periodontal Disease
Vitamin C
 Its deficiency in humans results in SCURVY a
disease characterized by hemorrhagic diathesis and
retardation of wound healing.
 Clinical manifestations
 Increased susceptibility to infections
 Impaired wound healing
 Bleeding and swollen gums
 Mobile teeth
Histopathological features
 Defective formation and maintenance of
collagen.
 Retardation or cessation of osteoid formation
and impaired osteoblatic function.
 Increased capillary permeability
 Suceptibility to traumatic hemorrhage
 Hyperactivity of contractile elements of the
peripheral blood vessels
 Sluggishness of blood flow.





Etiologic Relationships between Ascorbic Acid
and Periodontal Disease
Low levels of Ascorbic acid influences the
metabolism of collagen within the periodontium,
thereby affecting the ability of the tissue to
regenerate and repair by itself.
It interferes with bone formation leading to the loss
of the alveolar bone.
Increases the permeability of oral mucosa to
tritiated endotoxin and inulin.
Increased levels of Ascorbic acid enhances both the
chemotactic and migratory action of leukocytes
without influencing phagocytic activity.
Depletion of vitamin C may interfere with the ecologic
equilibrium of bacteria in plaque and increases its
pathogenicity.
Periodontal Features of Scurvy





The oral symptoms are same as chronic gingivitis
which can involve the attached gingiva and alveolar
mucosa.
In severe cases the gingiva becomes brilliant red
tender and grossly swollen.
The spongy tissues 'are extremly hyperemic and
bleed spontaneously.
In long standing cases the tissues attain a dark
blue or purple hue.
Alveolar bone resorption with indreased tooth
mobility has also been reported.
SCURVY
SCURVY IN SEVERE FORM
Vitamin D Deficiency
Vitamin D is essential for the absorption of calcium
from the gastrointestinal tract and the maintenance
of calcium phosphorus balance.
Radiographically
 There is a generalized partial to complete
disappearance of the lamina dura
 Reduced density of supporting bone ,loss of
trabeculae.
 Increased radiolucency of the trabecular interstices
and-increased prominenece of the remaining
trabelculane.

VITAMIN E


Evidence suggests that vitamin E acts as an
antioxidant. Severe familial neutropenia. and
plays an important role in maintaining the
stability of the cell mebrances and protecting
blood cells against hemolysis.
The possible role is based upon its ability to
interfere with the production of
prostaglandins.
VITAMIN A
 It is essential for normal functions of the retina,
for growth, differentiation and maintenance of
epithelial tissues and for bone growth and
embryonic development
VITAMIN B-COMPLEX
 Oral disease is rarely due to a deficiency in just
one component of the B-complex group. Oral
changes common to-Vitamin B-complex
deficiencies are gingivitis, glossitis, glossodynia,
angular chelitis and inflammation of the entire
oral mucosa.
METABOLIC AND ENDOCRINE
DISORDERS



The endocrine glands produce hormones that
control metabolism and maintain homeostasis.
Diabetes mellitus is the main endocrine disorder
that affects the periodontium.
The sex hormone can alter the response of
periodontal tissues to plaque. Disorders of the
pituitary, thyroid and adrenal glands have little
direct effect on the periodontal structures or in
altering the host response to bacterial plaque.
Diabetes Mellitus and
Periodontal Disease
Diabetic patient is more susceptible to periodontal
breakdown, which is characterized by extensive
bone loss, increased tooth mobility, widening of
periodontal ligament, suppuration and abscess
formation.
Pathogenesis
 There are several underlying factors that
accompany diabetes mellitus which may account for
the apparent increased prevalence of periodontal
disease in this condition. These factors are

1. Vascular changes:- Changes include thickening
and hyalinization of vascular walls, thickening of
capillary basement membranes, swelling and
occasional proliferation of the endothelial
cells, and splitting of capillary basement
membrane. Diabetic-induced changes in the
capillary basement membrane may have an
inhibitory effect on the transport of oxygen,
WBC, immune factors and waste products all of
which could affect tissue repair and
regeneration.
2. Impairment of PMN function is a feature of
diabetes mellitus. Disorders include reduced
phagocytosis and intracellular killing, impaired
adherence and impaired chemotactic response.
 Suggested causes include inhibition of the
glycolytic pathway with the PMNL’s abnormal
cyclic nucleotide metabolism, which disrupts the
organization of microtubules and
microfilaments, or a reduction in leukocyte
membrane receptors.
3. Biochemistry of crevicular fluid:- Alterations
in the constituents and flow rate of crevicular
fluid have been shown to be associated with
diabetes. Cyclic AMP levels seems to be
reduced in the diabetes group when
compared with control.
4. Changes in plaque microflora:- Studies have
indicated that proteolytic activity has not been
altered but hyaluronidase activity is lower in
plaque from diabetes.

severe gingival inflammation due to
diabetes
Bone loss in diabetes
PERIODONTAL ABSCESS FORMATION
Treatment
a. Periodontal treatment in patient with
uncontrolled diabetes is contraindicated.
b. If suspected to be a diabetic, following
procedures should be performed.
1.Consult the patients physician
2. Analyze laboratory tests blood glucose ,postprandial blood glucose, glycated hemoglobin,
glucose tolerance test (GTT), urinary
glucose.


If there is periodontal condition that requires
immediate care, prophylactic antibiotics
should be given.
If patient is a 'brittle' diabetic, optimal
periodontal health is a necessity. Glucose
levels should be continuously monitored
and periodontal treatment should be
performed when the disease is in a wellcontrolled state. Prophylactic antibiotics
should be started 2 days preoperatively,
Penicillin is the drug of first choice.
Guidelines
1. Clinician should make certain that the prescribed insulin has been
taken followed by a meal. Morning appointments, are ideal, after
breakfast because of optimal insulin levels.
2.After any surgical procedures, postoperative insulin dose should
be altered.
3. Tissues should be handled as atraumatically and as minimally
(less than 2 hours) as possible. For anxious patient's patient’s
preoperative sedation is required, epinephrine concentration
should not be greater than 1:1,00,000.
4.Diet recommendation should be made.
5.Antibiotic prophylaxis is recommended for extensive therapy.
6.Recall appointments and fastidious home oral care should be
stressed.
Thyroid Gland
Hypothyroidism leads to cretinism in children and
myxedema in adults. There are no notable
periodontal changes.



Treatment
Patients with thyrotoxicosis and those with inadequate
medical management should not receive periodontal therapy
until the condition is stabilized.
Medications such as epinephrine, atropine and other
pressor amines should be given with caution.
Hypothyroid patients require careful administration of
sedatives and narcotics because of their diminished ability to
tolerate drugs.
Pituitary Gland


Hyperpituitarism causes enlarged lips;
localized areas of hyper-pigmentation are
seen along nasolabial folds. It is also
associated with food impaction and hypercementosis.
Hypopituitarism leads to crowding and
malposition of teeth.
Parathyroid Glands


Parathyroid hypersecretion produces
generalized demineralization of the skeleton.
Oral changes include malocclusion and tooth
mobility, radiographic evidence of alveolar
osteoporosis, widening of the periodontal
space and absence of lamina dura.
Treatment: Routine periodontal therapy must
be instituted.


Gonads
There are several types of gingival diseases in which
modification of the sex hormones is considered to be
either an initiating or complicating factor; gingival
alterations are associated with physiologic hormonal
changes with a predominant marked hemorrhagic
tendency.
Gingiva in Puberty
Pronounced inflammation, bluish-red discoloration,
edema and enlarged gingiva may be seen.
Treatment: It is treated by scaling and curettage,
removal of all sources of irritation and plaque control. In
severe cases, surgical removal of enlarged tissue may
be required.

Gingival Changes Associated with
Menstrual Cycle
There is increased prevalence of gingivitis,
bleeding gingiva. Exudation from inflamed
gingiva is also increased, but the crevicular
fluid is not affected. The salivary bacterial
count is increased. No active treatment is
required.
Gingival Diseases in Pregnancy
 Pregnancy accentuates the gingival response
to plaque. The severity of gingivitis is
increased during pregnancy beginning, in the
second or third month. It becomes more
severe by the eight-month and decreases
during ninth month.
Clinical features
1.Pronounced base of bleeding.
2.Gingiva is bright-red to bluish-red.
3.Marginal and interdental gingiva is edematous,
pits on pressure and sometime presents
raspberry like appearance.

4.It has been suggested that during pregnancy
there is depression of maternal T-lymphocyte
response.
5.Aggravation of gingivitis has been attributed
principally to increased levels of
progesterone which produces dilatation and
tortuosity of the gingiva microvasculature,
circulatory stasis and increase susceptibility
to mechanical irritation.
6.Increased crevicular fluid flow, pocket depth
and mobility are also seen.
GINGIVA IN PREGNANCY
Treatment:



Requires elimination of all local irritants that are
responsible for precipitating gingival change.
Marginal and interdental gingival inflammations and
enlargement are treated with scaling and root
planing.
Treatment of tumor-like gingival enlargements
consists of surgical excision, scaling and planing of
tooth surfaces. In pregnancy emphasis should be
on:
Preventing gingival disease before it occurs.
Treating existing gingival disease before it becomes
worse.
Menopausal Gingivostomatitis

It occurs during menopause or in the
postmenopausal period. Clinical manifestations
include dry, shiny oral mucosa, dry burning
sensation of oral mucosa, abnormal taste
sensation described as salty, peppery or sour.
Effects of Hematological
Disorders on Periodontium

Disorders of the blood and blood forming
tissue can have profound effect on the
periodontal tissues and their response to
bacterial plaque. The WBC disorders have
the most pronounced effect on the
periodontal tissues. Disorders of hemostasis
can be classified according to the underlying
defect. There can be a defect in the vascular
constriction, platelet adhesion and
aggregation, coagulation and fibrinolysis.
White Blood Cell Disorders


The WBC’s disorders that affect the periodontium
can be categorized as either a disorder of
numbers or defect in function.
Neutropenias





Cyclic Neutropenia
Chronic benign neutropenia of childhood
benign familial neutropenia
Severe familial neutropenia
Chronic idiopathic neutropenia
Cyclic Neutropenia



It is characterized by a cyclic depression of the PMN
count in peripheral blood The cyclic intervals are
usually between 19 and 21 days. Clinical problems
include pyrexia, oral ulceration and skin infections.
Periodontal manifestations include oral ulceration,
inflamed gingiva, rapid periodontal breakdown, and
alveolar bone loss. Bone loss is most obvious around
the lower incisors and first permanent molars
Treatment: Plaque control, supportive measures like
antiseptic mouth wash, antimicrobial therapy has
been proposed.
Chronic Benign Neutropenia of
Childhood



The onset is usually between 6 to 20 months of age
and most patients, the condition is self-limiting
The main periodontal feature is brigt-red
hyperplastic, edematous gingivia confined to the
width of attached gingivia. THe gingival tissues
exhibit bleeding on probing and show areas of
desqumation, varying degrees of gingival recession
and pocketing are seen.
Treatment : Appropriate antimicrobial agent should
be prescribed.
Benign Familial Neutropenia

It is transmitted as an autosomal dominant trait. The
periodontal manifestations include hyperplastic
gingivliis exhibiting edematous and bright-red
appearance. There is marked bone loss around
the.fust molars. The gingival tissues bleed profusely
on probing

Treatment:
Plaque control and use of antimicrobial
mouth washes.


Chronic Idiopathic
Neutropenia
Thre is a persistent neutronpenia from birth and is
not cyclical. Clinical symptoms includes persistent
recurrent infections through out the patients life.
 Periodontal manfestions include persistent severe
gingivitis. The gingival is cherry – red edematous
and hypertrophic with occasional desquamation.
Treatment :
 Strict oral hygiene programme, scaling and regular
prophylaxis. Antiseptic irrigation and antibiotic are
advisable before tissue manipulation.

Leukemia



It is a malignant caused by proliferation of WBC forming
tissue, especially those in bone marrow. Acute
leukemia in more frequent in people under 20 years of
age. Chronic leukemia’s occur in people over 40 years
of age.
Periodontal Manifestations
The major manifestation being gingival enlargement,
gingival bleeding and periodontal infections. The
incidence and severity oof these problems varies
according to the type and nature of leukemia
a. Gingival enlargement is primarily due to a massive
leukemia cell infiltration into the gingival will hinder
mechanical plaque removal; hence there will be an
inflammatory component enhancing this
enlargement.
b. Gingival bleeding is a common oral manifestation of
acute leukemia. The bleeding is secondary to
thrombocytopenia that accompanies leukemia.
c. Infections of the periodontal tissues secondary to
leukemia can be of two types, either an
exacerbation of an existing periodontal disease or
an increased susceptibility of the periodontium to
fungal, viral or bacteria infections.
Treatment Plan for Leukemic
Patients
1. Refer the patient for medical evaluation and
treatment
2. Prior to chemotherapy, a complete periodontal plan
should be developed.
a. Monitor hematologic laboratory values.
b. Administer suitable antibiotics before any
periodontal treatment.
c. Periodontal treatment consist of scaling and root
planning, twice daily rinsing with 0.12 percent
chlorhexidine gluconate is recommended. If there is
irregular bleeding time, careful debridement with
cotton pellets soaked in 3 percent hydrogen
peroxide is performed.
3. During the acute phases of leukemia:
a. Cleanse the area with 3 percent hydrogen peroxide
(H2O2) or 0.12 percent chlorhexidine.
b. Carefully explore the area and remove any etiologic
local factors.
c. Re-cleanse the area with 3 percent H2 O2
d. Place a cotton pellet soaked in thrombin against the
bleeding point.
e. Cover with gauze and apply pressure for 15 to 20
minutes.


Acute gingival or periodontal abscesses are treated by
systemic antibiotics, gentle incision and drainage or by
treating with 3 percentage H2O2/0.12 percent
chlorhexidine gluconate.
Oral ulcerations should be treated with antibiotics and
mouth rinses.

In patients with chronic leukemia scaling
and root planning can be performed but
periodontal surgery should be avoided.
Plaque control and frequent recall visits
should receive particular attention.
Thrombocytopenic Purpura
It is characterized by a low platelet count, a prolonged clot retraction and
bleeding time, and a normal or slightly prolonged clotting time.
Clinical manifestations include spontaneous bleeding into skin or from
mucous membranes. Petechiae and hemorrhagic vesicles occur in the
cavity. Gingiva is swollen, soft and friable. Bleeding occurs spontaneously
Treatment
1. Physician referral for a definitive diagnosis.
2. Oral hygiene instructions.
3. Prophylactic treatment of potential abscesses.
4. No surgical procedures are indicated unless platelet count is at
least 80,000 cells/mm3.
5. Scaling and root planning may be carefully performed at low
platelet levels.
If surgery indicated, it shoud be as a traumatic as possible, stents or
thombin-soaked cotton pellets placed interproximally, gentle hydrogen
peroxide month washes and close post surgical follow – up is
recommended.
Disorders of WBC Function
Chediak-Higashi Syndrome


It is a rare familial and often fatal disease which is
transmitted as an autosomal recessive trait. PMNL’s
from patients with Syndrome show defective
migration defective chemo taxis, failure of post
phagocytic deregulation and diminished intracellular
bactericidal capacity.
Server gingival inflammation appears to be a
common finding in Chediak-Higashi syndrome. The
nature of the inflammatory charges may be plaque
induced, secondary to infection or related to the
underlying PMNL’s defect.
Lazy Leukocyte syndrome
 The featutre of the syndrome is a defect in
leukocyte chemotaxis and random mobility.
Marked gingivitis has also been described.
Chronic Granulomatous Disease
 A genetically-transmitted disorder
characterized by the inability of phagocytic
cells to destroy certain infecting microorganisms.
 Periodontal manifestations include marked,
diffuse, gingivitis with an accompanying
ulceration of buccal mucosa.
Red Blood Cell Disorders
Aplastic Anemia
 It is a bone marrow disorder characterized by a reduction in
hematopoietic tissue, bone marrow is replaced with fat and
pancytopenia. Bleeding from the gingival margins appears to be
a feature in these cases.
Fanconis Anemia
 This is a rare type of aplastic anemia characterized by a familial
bone marrow hypoplasia that becomes manifested in the first
decade of life. The periodontal manifestations being loss of
several teeth, severe bone loss with pocketing in excess of 10
mm. The gingiva will be bluish-red, bleed on probing, and shows
suppuration on gentle pressure.
APLASTIC ANEMIA
Sickle Cell Anemia
 In this condition, the red blood cells undergoes sickling
when subjected to hypoxia. Hence patients with sickle
cell anemias are susceptible to infections. In some
patients with sickle cell anemia, periodontal disease
may provide a sufficient inflammatory response to
precipitate a sickling crisis.
Acatalasia
 It is caused by a lack of the enzyme catalase in many
cells, especially the red blood cells and leukocytes. It
causes hypoxia and necrosis of the gingival tissues.
Severe periodontal destruction and gingival necrosis are
seen.
ANTIBODY DEFICIENCY DISORDERS
Acquired Immunodeficiency Syndrome

It is caused by a persistent HIV virus and is
characterized by destruction of lymphocytes,
rendering the patient susceptible to
opportunistic infections including destructive
periodontal lesions.
Clinical Manifestations
 HIV gingivitis: Persistent, linear, easily bleeding,
erythematous gingivitis has been described. Linear
gingivitis lesions may be localized or generalized in
nature. The erythematous gingivitis may be limited to
marginal tissue, or extend into attached gingiva in a
punctuate or a diffuse erythema or extend into alveolar
mucosa. A severely destructive, acutely painful
necrotizing ulcerative stomatitis has been reported.
 HIV periodontitis: NUP (Necrotizing ulcerative
periodontitis) is characterized by soft tissue necrosis
and rapid periodontal destruction that results in marked
interproximal bone loss. It is severely painful at onset.
KAPOSI’S SARCOMA IN AIDS
Treatment:
 Recommended management for linear gingival erythema
is as follows:
 Instruct the patient to perform meticulous oral hygiene.
 Scale and polish affected areas and perform
 subgingival irrigation with chlorhexidine.
 Prescribe chlorhexidine gluconate mouth rinse
 Reevaluation and frequent recall visits
 Systemic antibiotics such as metronidazole or amoxicillin
should be prescribed for patients with moderate to severe
tissue destruction. Use of prophylactic antifungal
medication should be considered.



PSYCHOSOMATIC DISORDERS
There are two ways by which psychosomatic
disorders may be induced in the oral cavity,
through the development of habits injurious to
the periodontium and by the direct effect of the
autonomous nervous system on the physiologic
tissue balance.
However, under the conditions of mental and
emotional stress, the mouth may subconsciously
become an outlet for the gratification of basic
drives in the adult. Gratification may be derived
from neurotic habits, which are potentially
injurious to the periodontium.
$
THANK YOU
$