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Title: ROLE OF SYSTEMIC DISEASE IN ETIOLOGY OF PERIODONTAL DISEASE


1
ROLE OF SYSTEMIC DISEASE
IN ETIOLOGY OF
PERIODONTAL DISEASE
2
  • 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.

3
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.

4
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

5
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.

6
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

7
  • 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.

8
  • 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.

9
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.

10
  • SCURVY

11
SCURVY IN SEVERE FORM
12
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.

13
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.

14
  • 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.

15
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.

16
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

17
  • 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.

18
  • 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 PMNLs abnormal
    cyclic nucleotide metabolism, which disrupts the
    organization of microtubules and microfilaments,
    or a reduction in leukocyte membrane receptors.

19
  • 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.

20
  • severe gingival inflammation due to
    diabetes

21
  • Bone loss in diabetes

22
  • PERIODONTAL ABSCESS FORMATION

23
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
    ,post-prandial blood glucose, glycated
    hemoglobin, glucose tolerance test (GTT), urinary
    glucose.

24
  • 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 well-controlled state. Prophylactic
    antibiotics should be started 2 days
    preoperatively, Penicillin is the drug of first
    choice.

25
  • 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 patients preoperative
    sedation is required, epinephrine concentration
    should not be greater than 11,00,000.
  • 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.

26
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.

27
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.

28
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.

29
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.

30
  • 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.

31
  • 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.

32
  • 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.

33
GINGIVA IN PREGNANCY
34
  • 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.

35
  • 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.

36
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.

37
White Blood Cell Disorders
  • The WBCs 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

38
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.

39
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.

40
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.

41
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.

42
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 leukemias 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

43
  • 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.

44
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.

45
  • 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.

46
  • 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.

47
  • 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.

48
Disorders of WBC FunctionChediak-Higashi
Syndrome
  • It is a rare familial and often fatal disease
    which is transmitted as an autosomal recessive
    trait. PMNLs 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 PMNLs defect.

49
  • 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 micro-organisms.
  • Periodontal manifestations include marked,
    diffuse, gingivitis with an accompanying
    ulceration of buccal mucosa.

50
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.

51
APLASTIC ANEMIA
52
  • 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.

53
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.

54
  • 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.

55
KAPOSIS SARCOMA IN AIDS
56
  • 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.

57
  • 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.

58
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