sys factors in etiology of pd disease

8/3/2019 Sys Factors in Etiology of Pd Disease

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ROLE OF SYSTEMIC

FACTORS IN ETIOLOGYOF PERIODONTAL

DISEASE

Presented by:Sonia Sachdeva

MDS II Prof


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INTRODUCTION


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Need for assessment of systemic factors To identify high-risk individuals inpriorso that preventiveand treatment procedures can be tailored to these individuals.

Only a subpopulation suffers from severe periodontal disease,systemic and other risk factors that are associated with thesevere periodontal disease in this subpopulation to beidentified public health measures can be rendered to

prevent periodontal disease in a cost-effective manner.


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CLASSIFICATION

NutritionalInfluences

EndocrineInfluences

HematologicDisorders

Genetic Disorders

Effect of systemic

drug therapy

Collagen Vascular

Diseases

Immunodeficiency

Disorders

Cardiovascular

Diseases

PsychosomaticDisorders

Other SystemicConditions-Metal

Intoxication

Systemic conditions & Systemic disorders

Various systemic factors that play role in etiology of periodontal disease are asfollows:


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ENDOCRINE DISORDERS


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ENDOCRINE DISORDERS Diabetes Hormonal fluctuations associated with puberty and pregnancy

Osteoporosis

Hyperparathyroidism

Endocrine disturbances and hormone fluctuations affect the periodontaltissues directly, modify the tissue response to local factors, and produceanatomic changes in the gingiva that may favor plaque accumulation anddisease progression


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DIABETES MELLITUS

2 main types:


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Diabetes & Periodontitis:

Considered the sixth complication of diabetes

More likely to occur in diabetic patients

Poorly controlled type 2 diabetics more likely to

develop periodontal disease than well-controlleddiabetics


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Study on Pima Indian population (Arizona) population with

highest prevalence of type 2 DM, the prevalence of

attachment loss and bone loss was greater among DMpatients than non DM patients in all age groups

DM subjects aged 15-34 years had mean attachment loss and

bone loss scores approx. twice as high as similarly aged nonDM subjects.

Mean %age of sites with >15% bone loss - 28% in wellcontrolled type 1 diabetes mellitus subjects

44% in poorly controlled diabetics.


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Mechanism of interaction in DM Changes in subgingival environmenti) Altered microbiotaii) Change in GCF composition

Altered tissue homeostasis and wound healingi) collagen production- alterations in wound healingii) MMP activityiii) Accumulation of AGEsiv) tissue turnover

Changes in host immunoinflammatory responsei) PMNL chemotaxis, adherance and phagocytosisii) pro-inflammatory cytokines response from monocyte /

macrophage

iii) tissue oxidant stress


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Response to Periodontal treatment inpatients with diabetes In well controlled DM, similar response to treatment is seen

(non DM).

In poorly controlled DM, less favourable response totreatment. In these, initial response to scaling and rootplaning is good, but chances of recurrence within 12 monthswas greater

Animal studies suggest decreased bone to implant contact inDM. the survival rate for implant was 90%, with failure rate of7.8% (DM) compared to 6.8% (Non DM) patients


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PUBERTY Increased testosterone (in males) and increased estradiol (in

females) is seen.

increased no. ofPrevotella Intermedia sp. seen , as they

substitute Progesterone & estrogen for menadione (VitaminK) as an essential nutrient.

increase in no. of Capnocytophaga species is seen,responsible for the increased bleeding tendency observedduring puberty .

Oral manifestations: Gingivitis, Recurrent apthous ulcers,Aggressive periodontitis (0.1% to 0.4%)


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Clinical features of puberty inducedgingivitis,

i) Marginal & interdental gingivalenlargement found primarily on thefacial surfaces, with lingual surfacesremaining relatively unaltered.

ii) increased gingival bleeding tendency

iii) increased inflammation with relativeless amounts of plaque

i) When puberty is passed, theinflammation tends to subside but doesnot disappear until adequate plaquecontrol is achieved.


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MENSTRUATION

During menstruation, changes seen are:

i) Gingivitis

ii) Increase in GCF flow

iii) Enlarged hemorrhagic gingiva in days preceding menstrual

flow

iv) Minor increase in Tooth mobility


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Muhlemann observed a case of bright red hemorrhagic lesionsof interproximal papilla prior to menstruation.

In addition to gingival inflammation

intraoral recurrent apthous ulcerationherpes labialis lesions

infections with Candida Albicans

are seen in some women and seem to be associated withincreased Progesterone levels during reproductive cycle.


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PREGNANCY During pregnancy, increased levels of sex steroid hormones--

in implantation of embryo, until parturition.

During pregnancy large quantities ofEstradiol (20mg/day),Estriol (80mg/day) and Progesterone (300mg/day) areproduced.

Direct relationship between Gingivitis and sustained, raised

levels of gestational hormones during pregnancy, withregression during the post partum period.


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You lose a tooth forevery pregnancy

Babies drain thecalcium from yourteeth

Every time you arepregnant your gumsbleed and you haveproblems with them

False to all:Meticulous oralhygiene with fluorideregimen will help toprevent all tooth and

gum problemsexperienced duringpregnancy


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Effects on Microbiota

Selective growth of periodontal pathogens i.e.P.Intermedia insubgingival plaque is seen during onset of pregnancygingivitis at 3 or 4 month of pregnancy- 55 fold increase

Gestational hormones act as growth factors, by satisfying thenapthoquinone requirement for bacteria.

Kornmann & Losche reported that during 2nd trimester,plaque levels remain constant, but gingivitis an gingivalbleeding increases in severity

Bacteroides melaninogenicus sp. also increases in pregnancy(55 fold) and in those taking contraceptives (16 fold)


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Effect on Tissues & Host response

Estrogen - sex steroid hormone responsible for alteration in

blood vessels in target tissues in females.

Increased Circulatory levels of Progesterone enhances capillarypermeability and dilatation, resulting in increased gingivalexudate

Increased Leakage of leukocytes and plasma proteins from postcapillary venules by affecting the endothelial lining, contributingto enhanced gingival inflammation.

Increased Progesterone levels the degree of keratinization ofgingival epithelium and alter the connective tissue groundsubstance.

Keratinization alongwith increased in epithelial glycogen

results in decreased effectiveness of the epithelial barrier


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Neutrophil chemotaxis and phagocytosis, alongwith T-cell

responses further causes the suppression of immune system toplaque.

Progesterone in particular stimulates the production ofinflammatory mediator PGE2 & increased accumulation of

PMNL in the gingival sulcus

IL-6 production by human gingival fibroblasts (upto 50%)

levels of Plasminogen activator inhibitor type 2 (PAI-2), animportant inhibitor of tissue proteolysis

CD3, CD4 and B lymphocytes during pregnancy, thus CD4/CD8ratio also decreases, leading to an immunodeficient state.

Peripheral blood lymphocytes showed a decreased response tobacterial antigens, in vitro, including extracts from P.intermedia


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Hormonal influences on cells ofperiodontium Sex steroid hormones directly or indirectly exert

influence on

cellular proliferation & differentiation growth in target tissues, including keratinocytes andfibroblasts in gingiva.

By altering collagen turnover, estrogens stimulateproliferation of gingival fibroblasts, and synthesis andmaturation of the gingival CT.


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These hormones also increase rate of folatemetabolism in oral mucosa.

Since folate is required for tissue maintenance,increased metabolism could deplete folate stores and

inhibit tissue repair.

During 3rd trimester, synthesis of GAGs a majorconstituent of CT matrix of gingiva, is reported.

In certain cases, estrogen and progesterone inhibitedcollagen synthesis by influencing the PDL fibroblastsin vitro.


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OSTEOPOROSIS Osteoporosis means literally _porous bone, a condition

where there is too little bone to provide mechanicalsupport.

Osteopenia- reduction in bone mineral density belowwhat is required for mechanical support.


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WHO Diagnostic Guidelines forInterpretation of Bone MassMeasurements in Caucasian Women Severe Osteoporosis

BMD more than 2.5 standard deviations (SD) below themean value of peak bone mass in young normal womenand the presence of fractures.

OsteoporosisBMD more than 2.5 SD below the mean value of peak

bone mass in young normal women. Low bone mass (Osteopenia)

BMD within 1 SD and 2.5 SD of the mean value of peakbone mass in normal young women

NormalBMD not more than 1SD below mean value of peak bonemass in young normal women.


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Classification of Osteoporosis Primary Idiopathic Juvenile

Adult Secondary

Endocrine disorders-Diabetes mellitusGastrointestinal and malabsorption syndromesMyeloproliferative disorders

Multiple myelomaConnective tissue diseases Marfan syndrome Ehlers-Danlos syndrome

Chronic Obstructive Pulmonary disease


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Common Risk Factors

Osteoporosis Periodontal Disease

Hereditary/genetics Female gender AgeCaucasian or Asian race Race

Family history Familial aggregation

Menopause IL-1 polymorphism

Petite body build

Suboptimal peak bone mass

Dietary factors Low intake calcium Low intake calciumLow intake vitamin D Low intake vitamins C, E

High intake caffeine, protein,

salt, phosphate

Environment Smoking Smoking

Alcohol Alcohol

Physical inactivity StressSystemic factors Diabetes mellitus Diabetes mellitus

Multiple myeloma Osteoporosis


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Periodontal disease and osteoporosis Relationship of tooth loss and BMD has been studied.

Several reports find a correlation between tooth loss and

diminished systemic BMD.Other reports fail to find thiscorrelation.

The use of tooth loss as a surrogate for periodontal disease extent

has several limitations.

Underlying reason for the loss of the teeth is often unknown.

The extent of the disease around the remaining teeth is not takeninto account in these analyses.


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HORMONALCONTRACEPTIVES

Contraceptives utilize synthetic gestational hormones(estrogen and progesterone), to reduce the likelihood ofovulation/implantation (Guyton 1987).

Less dramatic but similar effects to pregnancy are sometimesobserved in the gingivae of hormonal contraceptive users.

The most common oral manifestation of elevated levels of

ovarian hormones is an increase in gingival inflammationwith an accompanying increase in gingival exudate (Mariotti1994).


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Effect on tissue response Both estrogen and progesterone increase gingival exudate, associated with

inflammatory edema (Lindhe & Bjorn 1967).

A 53% increase in crevicular fluid volume has been demonstrated inhormonal contraceptive users compared with controls.

Human gingiva has receptors for progesterone and estrogen (Vitteket al.1982; Staffolani et al. 1989), providing evidence that gingiva is a targettissue for both gestational hormones.

Progesterone causes increased vascular permeability, resulting in theinfiltration of polymorphonuclear leukocytes and raised levels of PGE2 inthe sulcular fluid (Miyagi et al. 1993).

Increased capillary permeability may be induced by estrogen by stimulatingthe release of mediators such as bradykinin, prostaglandins, and histamine.However, the main effects of estrogen are in controlling blood flow.

Hence the combination of estrogen and progesterone in the contraceptivepill can contribute to vascular changes in the gingivae. The resultantgingivitis can be minimized by establishing low plaque levels at thebeginning of oral contraceptive therapy (Zachariasen 1993).


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HYPERPARATHYROIDISM

Osteitis fibrosa cystica or von Recklinghausen's bone disease

Generalized demineralization of the skeleton

increased osteoclasis with proliferation of the connective tissue inthe enlarged marrow spaces

formation of bone cysts and giant cell tumors.


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Oral changes- malocclusion and tooth mobility

radiographic evidence of alveolar osteoporosiswith closely meshed trabeculae

widening of the pdl space

absence of the lamina dura radiolucent cyst like spaces- brown tumors

Different investigators report that 25%, 45%, and50% of patients with hyperparathyroidism haveassociated oral changes.


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NUTRITIONAL INFLUENCES


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i) Nutritional deficiencies that produce changes in the oral cavity.

These changes include alterations of the lips, oral mucosa andbone as well as of the periodontal tissues.

ii) These changes are considered to be periodontal or oralmanifestations of nutritional disease.

iii) There are no nutritional deficiencies that by themselves cancause gingivitis or periodontal pockets.


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Nutritional influences

Physicalcharacter of

diet

Effect onoral

microbes

Deficiencyof specific

components

Effect on microbes

distributionof types oforganisms

metabolicactivity &

pathogenicpotential,

Sources of nutrients:

Endogenous Exogenous


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FAT-SOLUBLE VITAMIN DEFICIENCY

VITAMIN A DEFICIENCY. Dermatologic, mucosal, and ocular manifestations. Degenerative changes occur in epithelial tissues

keratinizing metaplasia.

Periodontal changes Animal studies: Hyperplasia and hyperkeratinization of the

gingival epithelium with proliferation of the junctionalepithelium and retardation of gingival wound healing. In the

presence of local factors, vitamin A-deficient rats developdeep periodontal pockets.

Humans: No relation between this vitamin and periodontaldisease.


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VITAMIN D DEFICIENCY.

Animal studies (young dogs):

osteoporosis of alveolar bone osteoid that forms at a normal rate but remains uncalcified failure of osteoid to resorb reduction in the width of the periodontal ligament space a normal rate of cementum formation, but defective calcification

and some cementum resorption Distortion of the growth pattern of alveolar bone.

Osteomalacic animals: Rapid, generalized, severe osteoclasticresorption of alveolar bone, proliferation of fibroblasts that replacebone and marrow, and new bone formation around the remnants ofunresorbed bony trabeculae.

Radiographically: generalized partial to complete disappearance ofthe lamina dura, loss of trabeculae, increased radiolucence of thetrabecular interstices, and increased prominence of the remainingtrabeculae.


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WATER-SOLUBLE VITAMIN DEFICIENCY

B-COMPLEX DEFICIENCY.

Oral changes common to B-complex deficiencies

Gingivitis- non-specific, as it is caused by bacterial plaquerather than by the deficiency.

Glossitis

Glossodynia

Angular cheilitis Inflammation of the entire oral mucosa.


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VITAMIN B1

Oral disturbances:

Hypersensitivity of the oralmucosa

Minute vesicles (simulatingherpes) on the buccal mucosa,under the tongue, or on thepalate.

Erosion of the oral mucosa


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VITAMIN B2 Glossitis; angular cheilitis;

seborrheic dermatitis; andsuperficial vascular keratitis.

Glossitis is characterized by amagenta discoloration and atrophyof the papilla.

In mild to moderate cases, dorsumexhibits a patchy atrophy of thelingual papilla and engorgedfungiform papilla, which project as

pebble like elevations.

In severe deficiency, the entiredorsum is flat, with a dry and oftenfissured surface.

FISSURED TONGUE


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Angular cheilitis, begins as aninflammation of the commisureof the lips, followed by erosion,

ulceration and fissuring.

D/D Angular Cheilitis due to

decreased VD in dentures

Candidiasis (Perleche)

Supplemental riboflavin isineffective to resolve cases of

glossitis and angular cheilitis thatare not caused by vitamindeficiency.

ORAL ULCERATION

ANGULAR CHEILOSIS


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VITAMIN B3

Pellagra : diarrhea, dermatitis and dementia.

Glossitis and stomatitis may be the earliest signs of niacindeficiency. The gingiva may be involved in ANIACINOSIS

with or without tongue changes. Most common finding isNUG usually in areas of local irritation.

Oral manifestations in experimental animals :

Black tongue Gingival inflammation with destruction of gingival,

periodontal ligament and alveolar bone. Necrosis of the gingiva and other oral tissues and

leucopenia are the terminal features of niacindeficiency.


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BIOTIN DEFICIENCY

Oral signs of biotin deficiency are

pallor of the tongue, and

patchy atrophy of the lingualpapilla.

Although the pattern resemblesgeographic tongue, it is confinedto the lateral margins or isgeneralized to the entire dorsum.


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FOLIC ACID DEFICIENCY

Macrocytic anemia with megaloblastic erythropoeisis,accompanied by oral changes , gastrointestinal changes, diarrheaand intestinal malabsorption.

Folic acid deficient animals demonstrate necrosis of gingiva,periodontal ligament and alveolar bone without inflammation.The absence of inflammation is due to deficiency inducedgranulocytopenia.

In humans with sprue and other folic acid deficient states,generalized stomatitis occur, accompanied by ulcerated glossitisand cheilitis.


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Fiery red tongue completelyDevoid of papilla

Folic acid deficiency


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VITAMIN B12 DEFICIENCY

A deficiency of vitamin B12 is rarely caused by insufficientdietary sources unless strict vegan diets are followed.

Lack of intrinsic factor is the primary cause of deficiency.

Pernicious anemia (a megaloblastic anemia) occursfrequently in the elderly relative to achlorhydria anddecreased synthesis of intrinsic factor by the parietal cells.

Deficiency symptoms develop very slowly.


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Initial oral symptoms develop withGlossopyrosis followed by swelling and pallorwith eventual disappearance of the filiformand fungiform papilla.

The tongue may be completely smooth, shinyand deeply reddened with loss or distortion oftaste.

Bright red, diffuse, excruciating painful lesionsmay occur in the buccal and pharyngealmucosa and undersurface of the tongue.

stomatitis or a pale or yellowish mucosa,xerostomia, cheilosis, hemorrhagic gingival

and bone loss. Neurological symptoms like numbness or

tingling, occur as a consequence ofdemyelination of nerves.


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VITAMIN C

Vitamin C deficiency in humans result in scurvy, a diseasecharacterized by hemorrhagic diathesis and retardation ofwound healing.

Clinical manifestations

Increased susceptibility of infections Impaired wound healing Bleeding and swollen gums Mobile teeth Hemorrhagic lesions into the muscles of

extremities, joints and sometimes nail beds Petechial hemorrhages often around hair follicles


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Possible etiologic relationships between ascorbic acid and

periodontal disease

Low levels of ascorbic acid influences the metabolism of collagen withinthe periodontium, thereby affecting the ability of the tissue toregenerate & repair by itself.

It interferes with bone formation leading to the loss of alveolar bone.

Increases the permeability of oral mucosa to tritiated endotoxin andtritiated inulin and of normal crevicular epithelium to tritiated dextran.

Optimal levels of ascorbic acid is required to maintain the integrity ofthe periodontal microvasculature as well as the vascular response to

bacterial irritation and wound healing.

Depletion of vitamin C may interfere with the ecologic equilibirium ofbacteria in plaque and increase its pathogenicity.


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Histopathological features

Defective formation and maintenance of collagen

Retardation or cessation of osteoid formation & impairedosteoblastic function

Increased capillary permeability

Susceptibility to traumatic hemorrhages

Hyporeactivity of contractile elements of the peripheral blood

vessels

Sluggishness of blood flow

PMNs affected


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GINGIVITIS IN VIT.C DEFICIENCY

Gingivitis with enlarged, hemorrhagic, bluish red gingiva isdescribed as one of the classic signs of vitamin C deficiency,

Gingivitis is not caused by vitamin C deficiency.

Vitamin C deficiency may aggravate the gingival responseto plaque and worsen the edema, enlargement andbleeding.


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PROTEIN DEFICIENCY

Hypoproteinemia- muscular atrophy, weakness, weight loss,anemia, leucopenia, edema, impaired lactation, decreasedresistance to infection slow wound healing, lymphoid depletion

and reduced ability to form certain hormones and enzymesystems.

Changes in periodontium In the periodontium of experimental animals:

Degeneration of the connective tissue of the gingiva andperiodontal ligament, osteoporosis of alveolar bone retardationin the deposition of cementum, delayed wound healing.


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STARVATION

In a study of controlled semistaravation in young adults there wereno changes in the oral cavity or skeletal system despite a 24% loss ofbody weight.

Another study showed a reduction in plaque index scores and aconsiderable increase in gingival index scores as the fasting periodlengthened.

In experimental animals, acute starvation results in osteoporosis ofalveolar bone and other bones, reduction in the height of alveolarbone and accentuated bone loss associated with gingivalinflammation.


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HEMATOLOGIC DISORDERS


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REDBLOODCELLDISORDERS

Anemia

Pernicious anemia- Tongue changes in 75% of cases.Tongue appears red, smooth, and shiny, owing to atrophy ofthe papillae. Marked pallor of the gingiva.

Iron deficiency anemia induces similar tongue and gingivalchanges- Plummer-Vinson syndrome

Sickle cell anemia - Oral changes include generalizedosteoporosis of the jaws, with a peculiar stepladderalignment of the trabeculae of the interdental septa, alongwith pallor and yellowish discoloration of the oral mucosa.Periodontal infections may precipitate sickle cell crisis.

Aplastic anemias - Oral changes include palediscoloration of the oral mucosa and increased susceptibilityto infection, owing to the concomitant neutropenia.


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Acatalasia or acatalasemia

Rare, inherited (autosomal recessive) disorder caused by the lackof catalase in cells, especially red and white blood cells.

The neutralisation of catalase protects these cells from harmfuloxidising agents which could denature haemoglobin and produce

local hypoxia and necrosis of the gingiva.

A report by Delgado and Calderon(1979) indicated severeperiodontal destruction and gingival necrosis is likely in thesepatients.

While patients with acatalasia are not generally prone toinfections, approximately 2550% suffer an oral condition calledTakaharas disease, characterized by painful ulcerations of thegingiva and tonsillar lacunae.


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WHITEBLOODCELLS

Quantitative leucocyte disordersNeutropenia: Neutrophil count falls below 1,000 cells/ml.

An absolute neutrophil count less than 200 cells/ml corresponds with aninability to mount an inflammatory response.

Cyclic neutropenia:Periodontal manifestations- inflamed gingiva,gingival ulceration, periodontal attachment and bone loss.

Familial neutropenia:Periodontal manifestations- fiery redoedematous gingivitis, which is often hyperplastic and accompanied

by periodontal bone loss.

Kirstila et al (1993) described a Finnish family with three adolescentsiblings affected by neutropenia. Two of the siblings had severeperiodontitis and the other sibling presented with oral ulceration.


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Leukaemia

Gingival tissues are considered more susceptible to leukaemic cellinfiltration.

Gingival bleeding is also a common sign in both acute and chronic

leukaemia.

In some cases there is rapid loss of alveolar bone, usually due toexacerbation of pre-existing periodontitis or as a result ofchemotherapy or radiotherapy treatment regimes.

Clinical periodontal features include anaemic pallor of thegingivae, bleeding due to platelet deficiency and reduced resistanceto infection due to decreased immune and inflammatory cellnumbers.


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Periodontium in Leukemic Patients

Oral and periodontal manifestations of leukemiaconsist of

Leukemic infiltration Bleeding

Oral ulcerations & infections.


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Leukemic Infiltration of Periodontium

Leukemic cells can infiltrate the gingiva and, lessfrequently, the alveolar bone. Gingival infiltration oftenresults in leukemic gingival enlargement.

Leukemic gingival enlargement consists of a basic infiltration

of the gingival corium by leukemic cells that creates gingivalpockets where bacterial plaque accumulates, initiating asecondary inflammatory lesion that contributes also to theenlargement of the gingiva.

Gingiva appears initially bluish red and cyanotic, with arounding and tenseness of the gingival margin; then itincreases in size, most often in the interdental papilla andpartially covering the crowns of the teeth.


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Bleeding.

Bleeding gingiva can be an early sign of leukemia.

Due to the thrombocytopenia that results fromreplacement of the bone marrow cells by leukemic cells

and also from the inhibition of normal stem cell functionby leukemic cells or their products.

This bleeding tendency can also manifest itself in theskin and throughout the oral mucosa, where petechiae

are often found, with or without leukemic infiltrates.

Oral bleeding has been reported as a presenting sign in17.7% of patients with acute leukemia and in 4.4% ofpatients with chronic leukemia.


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Oral Ulceration and Infection.

Granulocytopenia resulting from the replacement of bone marrowcells by leukemic cells reduces the tissue resistance to opportunistic

microorganisms and leads to ulcerations and infections.

These lesions occur in sites of trauma such as the buccal mucosa inrelation to the line of occlusion or the palate. Acute gingivitis andlesions of necrotizing ulcerative gingivitis are more frequent and

severe in terminal cases of acute.

The inflamed gingiva differs clinically from inflamed gingiva innonleukemic individuals. It is a peculiar bluish red, is markedlysponge like and friable, and bleeds persistently on the slightest

provocation or even spontaneously.

This markedly altered and degenerated tissue is extremelysusceptible to bacterial infection, which can be so severe as to causeacute gingival necrosis and pseudomembrane formation.


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Classification for the aetiology of gingivallesions in leukaemic patients has been proposed

by Barrett.(1984) .

Category 1 is concerned with lesions caused by directleukaemic infiltration and includes gingival enlargement.

Category 2 deals with direct drug toxicity caused bychemotherapeutic agents.

Category 3 comprises the detrimental effects of graft-versus-host reactions. In this disease, the transplanted lymphocytesreact against host antigens.

Category 4 involves secondary effects from the depression ofmarrow/lymphoid tissue and includes haemorrhage,neutropenic ulceration and an increased susceptibility tomicrobial infections.


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Qualitative disorders

Neutrophil dysfunction Qualitative disorders of neutrophil function also

increase the hosts susceptibility to infection.

Classification of neutrophil disorders correspondswith the major neutrophil processes: margination(rolling and adhesion), chemotaxis and migration,phagocytosis, degranulation and killing.

Defects in the process of margination: LAD I &LADII Defects in intracellular killing: Chediak Higashi

Syndrome


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PLATELETS

Thrombocytopenia

Thrombocytopenic purpura - Low platelet count, a prolongedclot retraction and bleeding time, and a normal or slightlyprolonged clotting time.

There is spontaneous bleeding into the skin or from mucousmembranes. Petechiae and hemorrhagic vesicles occur in theoral cavity, particularly in the palate, tonsillar pillars, and thebuccal mucosa.

The gingivae are swollen, soft, and friable. Bleeding occursspontaneously or on the slightest provocation and is difficult

to control.

Gingival changes represent an abnormal response to localirritation; the severity of the gingival condition isdramatically alleviated by removal of the local factors.


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IMMUNODEFICIENCY DISORDERS

Agranulocytosis.

Ulceration in the oral cavity, oropharynx, and throat ischaracteristic. The mucosa exhibits isolated necrotic patches

that are black and gray and are sharply demarcated from theadjacent uninvolved areas.

The absence of a notable inflammatory reaction due to lackof granulocytes is a striking feature.

The gingival margin may or may not be involved. Gingivalhemorrhage, necrosis, increased salivation, and fetid odor areaccompanying clinical features. The occurrence of rapidlydestructive periodontitis has been described in cyclicneutropenia.


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ANTIBODYDEFICIENCYDISORDERS Agammaglobulinemia. Agammaglobulinemia results from a

deficiency in B cells; T-cell function remains normal. It can becongenital (X-linked or Bruton's agammaglobulinemia) oracquired. The disease is characterized by recurrent infections,including destructive periodontitis in children

ACQUIRED IMMUNODEFICIENCYSYNDROME. Acquired

immunodeficiency syndrome (AIDS) is caused by the humanimmunodeficiency virus (HIV) and is characterized bydestruction of lymphocytes, rendering the patient susceptibleto opportunistic infections, including destructive periodontallesions and malignancies.


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CARDIOVASCULAR DISEASE


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CARDIOVASCULAR DISEASES

ArteriosclerosisCongenital Heart

Disease

Tetralogy ofFallot

EisenmengersSyndrome


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ARTERIOSCLEROSIS

Both periodontal disease and arteriosclerosis increase with age.

Circulatory impairment induced by vascular changes may increase thepatient's susceptibility to periodontal disease.

Conversely, there is recent evidence to suggest that individuals withperiodontal disease may be at greater risk for heart disease as a result of

chronic periodontal infections and inflammation.

In experimental animals, partial ischemia of more than 10 hours' durationcreated by arteriolar occlusion produces changes in the oxidative enzymesand acid phosphatase activity and in the glycogen and lipid content of thegingival epithelium. Focal necrosis, followed by ulceration, occurs in theepithelium, with the junctional epithelium least affected.

Changes typical of periodontal disease do not occur. Ischemia is followed byhyperemia, which is accompanied by metabolic changes and increased DNAsynthesis in the epithelium. The gingival response to arteriolar occlusion isepithelial proliferation and thickening.


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Tetralogy of Fallot

1. Ventricular septal defect2. pulmonary stenosis3. malposition of the aorta to the right4. Compensatory right ventricular enlargement.

The oral changes include a purplish red discoloration of thelips and gingiva and sometimes severe marginal gingivitis andperiodontal destruction.

The discoloration of the lips and gingivae corresponds to thegeneral degree of cyanosis and returns to normal after

corrective heart surgery.

The tongue appears coated, fissured, and edematous, andthere is extreme reddening of the fungiform and filiformpapillae.


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Eisenmengers Syndrome

Among patients with ventricular septal defects, about halfwith large defects (>1.5 cm in diameter) develop Eisenmengersyndrome. This syndrome is distinguished by a greater bloodflow from stronger left ventricle to the right ventricle(backward flow) through the septal defect causing increasedpulmonary blood flow, which in turn leads to progressive

pulmonary fibrosis, small vessel occlusion, and highpulmonary vascular resistance.

The natural history of a patient with untreated Eisenmengerssyndrome is a gradual increase in cyanosis over many years,eventually leading to cardiac failure.

In casesofEisenmenger syndrome, the lips, cheeks, andbuccal mucous membranes are cyanotic, but markedly less sothan in tetralogy of Fallot. Severe generalized marginalgingivitis may be found.


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GENETIC DISORDERS


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GENETIC DISORDERS

Connective tissue alterations:

Marfan syndrome

Ehler-Danlos syndrome.

Immune alterations

severe congenitalneutropenia

infantile genetic agranulocytosis orKostmann syndrome (IGA)

Chediak-Higiashi syndrome

Down syndrome

Papillon-Lefvre syndrome

hyperimmunoglobulinemia E syndrome


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2.Marfan Syndrome

Generalized disorder of connective tissue with skeletal,ocular, and cardiovascular malformations.Characteristically these patients are tall and thin with

arachnodactyly and joint hypermobility.

In the case of Marfan syndrome, periodontitis manifestsin a chronic and severe form with patterns of bothhorizontal and vertical bone resorption, and in

accordance to the presence of bacterial plaque.

Dental mobility has been shown to be due toperiodontitis, and is not attributable to the primarycondition of the syndrome.


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GENETICDISORDERSRESULTINGINIMMUNEALTERATIONS1. Downs Syndrome Periodontal disease is characterized by a generalized

early periodontitis, which commences in the deciduousdentition and continues into the adult dentition.

Even though oral hygiene of these patients is poor theperiodontal destruction in these patients exceeds thatexplainable by local factors alone.

Periodontal disease is characterized by

Deep periodontal pocket moderate gingivitis Commonly seen in lower anterior region Marked recession associated with high frenal attachment Acute necrotizing lesion is a frequent finding


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The high prevalence of periodontitis in downsyndrome patients is explained by

a. Reduced resistance due to poor circulationespecially in those area of terminalvascularization such as gingival tissue and defectin T cell maturation and PMN chemotaxis

b. Increase in number of P. intermedia in mouthsof children with down syndrome


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2. Leukocyte Adhesion Deficiency

Syndrome Autosomal recessive disease.

Deficiencies in expression of the LeucocyteFunction Adhesion family of adhesins.

Children with deficiencies in expression of the

Leucocyte Function Adhesion family of adhesinshave been reported as suffering from severeperiodontal infections, data relating adultperiodontitis to this condition are not available.


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3. Papillon-Lefevre syndrome

An autosomal recessive disease due to mutation in the cathepsin C gene

Etiology is variable --deficits in chemotaxis, phagocytosis andintra cellular killing.

Hyperkeratosis of palms and soles

Generalised rapid destruction of the periodontal attachment apparatus,resulting in premature loss of both the dentitions.

Other findings:

Ectopic calcification of falx ceribri and choriod plexus.Increased susceptibility to infectionsMental retardationEndocrine disorders

Aggressive periodontitis


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4. Chediak Higashi Syndrome

Rare autosomal recessive disorder affecting neutrophils, due tomutation in the vesicle trafficking regulatory gene.

Manifests early in life as Occulo cutanous albinism

Photophobia Pyogenic infections and lymph adenopathy

Oral findings include 1. Gingivitis 2. Ulcerations of both tongue and buccal mucosa 3. Early onset periodontitis leading to loss of both the dentitions.

Hallmark-large Azurophilic granules in the cytoplasm of theneutrophils.- impair neutrophil migration which causes neutrophilsunable to phagocytose microbes.


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5. Hypophosphatasia

Patients with this condition have a decreased serum alkalinephosphatase and severe loss of alveolar bone and prematureloss of the deciduous teeth, particularly anteriorly.

Microscopically, the teeth show either complete loss of

cementum or isolated areas of cementum resorption.


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8. Lazy leukocyte syndrome

An extremely rare disorder that manifests in both quantitativeand qualitative neutrophil defects.

Recurrent infections due to both a deficiency in neutrophilchemotaxis and a systemic neutropenia.

Impaired random and directional motility leads to adiminished in vivo migration of neutrophils into the tissue

and to sites of inflammation.


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9. Chronic Granulomatous Disease

Rare disease with 2 genetic forms, autosomal recessive and X-linked recessive.

The defect in this disease is in the ability of phagocytic cells toperform killing by the oxidative pathway after ingestion.

Kinane (1990) described a family with the X-linked recessiveform of chronic granulomatous disease. Erythema of thegingiva and oral mucosa with occasional ulceration were seen,no periodontal manifestations were attributable to thiscondition.


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10. Glycogen storage disease type 1b

Autosomal recessive disorder caused by a defect in the glucose-6-phosphate transporter protein.

Clinical features :dolllike facial appearance, stunted growth,hypoglycemia, ketosis, lactic acidosis, hyperlipidemia, gout, andbleeding episodes brought on by impaired platelet functionsecondary to metabolic disorders.

Additional distinguishing features of glycogen storage disease

type 1b are neutropenia, neutrophil dysfunction, and anincreased susceptibility to infection.

Defects in both random and directed PMN migration.


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Reports of oral disease in glycogen storage disease type 1bpatients are common & include:

Oral Ulceration

Candidiasis

Gingivitis And Periodontitis.

Dougherty & Gataletto described a case of generalizedaggressive periodontitis in a child with glycogen storagedisease type 1b.


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EFFECT OF SYSTEMIC DRUGTHERAPY


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PHENYTOIN INDUCED ENLARGEMENT


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COLLAGEN VASCULAR DISORDERS


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SJOGRENSSYNDROME

dryness of the eyes and mouth.Primary -sicca

syndrome

triad of dry eyes with keratoconjunctivitis sicca,xerostomia and an associated autoimmunedisease, usually rheumatoid arthritis

Secondary form

2.2 higher risk of having adult periodontitis.Study by Najera

et al (1997)


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RHEUMATOIDARTHRITISOccurrence ofSjogrens syndrome in approx. 15% of such

patients.

More than 50% ofSjogrens patients are affected by rheumatoidarthritis.

deterioration of TMJ

loss of vertical dimension of the condyle anterior open bite.

excessive occlusal forces in the molar regions

lost bone support from extrusion of the anterior teeth.


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LUPUSERYTHEMATOSUS chronic autoimmune disease that affects the connective tissue

and multiple organ systems.

An increased incidence of infection in systemic lupuserythematosus patients is an often-reported finding. It isestimated that at least 50% of systemic lupus erythematosuspatients will suffer an infection during the course of thedisease.

Hematologic disorders that may explain this increasedincidence of infection are a tendency to neutropenia and

various neutrophil abnormalities.

oral manifestation - formation of multiple white plaques withdark, reddish or purple margins with a tendency to formtelangiectasia and ulceration.


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little information on the periodontal status of systemic lupuserythematosus patients.

In an uncontrolled study of 16 women with systemic lupuserythematosus, Rhodus & Johnson found periodontitis in all

but one of them.

Novo et al. observed periodontitis in 60% of 30 systemic lupuserythematosus patients compared to 50% in a control groupwith rheumatoid arthritis.

In a comparison of the periodontal status of systemic lupuserythematosus patients with age and sex-matched controls,Mutlu et al. found that the SLE patients had significantlyshallower probing depths than the control group.


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PROGRESSIVESYSTEMICSCLEROSISAND

CREST SYNDROME Most conspicuous oral manifestation - fibrosis of the facial

skin to affect 35% ofSjogrens syndrome patients. 39% ofpatients complained of dysphagia and 28% reported limitedmouth opening as a consequence of the sclerosis.

The advanced progression of facial tissue fibrosis has beendescribed as the cause for resorption of the mandibular bonein the area of the mandibular angles .

A relatively characteristic oral manifestation of progressivesystemic sclerosis is the radiographic demonstration ofapparent widening of the periodontal ligament space. Thistypically affects posterior teeth and the pdl space may beincreased as much as 3-4 times the normal thickness.


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Uniform widening of pdl space in systemic sclerosis


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PSYCHOSOMATIC DISORDERS

Harmful effects that result frompsychic influences on the organic

control of tissues are known aspsychosomatic disorders


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2 ways in which psychosomatic disorders may be

induced in the oral cavity are:

1. through the development of habits that areinjurious to the periodontium.

1. by the direct effect of the autonomic nervoussystem on the physiologic tissue balance.


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PSYCHIATRICINFLUENCEOFSELFINFLICTEDINJURY

under conditions of mental and emotional stress, themouth may subconsciously become an outlet for thegratification of basic drives in the adult.

Gratification may be derived from neurotic habits, suchas grinding or clenching the teeth; nibbling on foreignobjects (e.g., pencils or pipes); nail biting; or excessiveuse of tobacco, which are all potentially injurious to the

periodontium.

Self-inflicted gingival injuries such as gingival recessionhave been described in both children and adults.


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SELF INFLICTED INJURY ON GINGIVA DUE TO SCRATCHING OF AREA


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GINGIVITIS

Stress diminishes saliva flow and increases dental plaque formation.

Emotional stress modifies the saliva pH and its chemicalcomposition like the IgA secretion.

Deinzer et al. (1999-2001)- examined the impact of academic

stress by students at university during their examination period onperiodontal health. Academic stress was shown to be a risk factorfor gingival inflammation with increasing crevicular interleukin-1levels and a diminution of the quality of the oral hygiene.

In a pilot study in 1998, Axtelius showed the presence of cortical in

gingival crevicular fluid.

A study by Johanssen (2006) confirm the fact that theconcentration of cortisol in the gingival crevicular fluid is higherby person showing depression signs.

N


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NECROTIZING PERIODONTALDISEASES

The first reports were written about mouth pain among thesoldiers of Alexander the Great.

The first studies showing this influence were made by Pindborg(1951) (higher number of necrotic periodontitis during militaryservice) and in 19631964 by Giddon (more necrotic periodontitisin college during examination period).

The presence of NUG in soldiers stressed by war time conditions inthe trenches lead to one of the early diagnostic terms used todescribe this condition, trench mouth.

The main risk factors for necrotic periodontitis and previousepisode are: past episode of necrotic periodontitis, bad oralhygiene, bad sleep, unusual emotional stress, tobacco, alcohol,bad alimentation and recent illness. Many of those factors are oftenrelated to stress.


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CHRONIC PERIODONTITIS

Linden et al. predicted the future attachment loss dependingon the following criteria: age, socio-economical level, a lesssatisfactory professional life and a passive and dependantcharacter.

Axtelius (1998) has suggested that patients withpsychosocial strain and passive dependent traits didnot respond as well as patients with less stressfulpsychosocial situation and with a rigid personality to

periodontal treatment.

The real relationship between stress and chronicperiodontal disease is difficult to establish and moreresearch needs to be done.


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PERIODONTALTREATMENT

Kamma and Baehni- supportive periodontal care was more effective inpatients with aggressive periodontitis harbouring less stress.

Wimmer et al. explain the influence of coping with stress onperiodontal therapy and conclude that patients with maladaptativecoping strategies have more advanced disease and poor response to anon-surgical periodontal treatment.

Thus maladaptative behaviors, especially in association with other riskfactors (like smoking) are of great importance in the medical history,treatment and maintenance of patients with periodontal disease.

Gamboa et al. (2005), show the influence of Emotional Intelligence (ameasure of the coping mechanisms) on the initial responses toperiodontal treatment in patients with chronic periodontitis.Reductions of dental plaque and gingival bleeding were positivelycorrelated in patients having an active coping


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OTHER SYSTEMIC CONDITIONS

METALINTOXICATION


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Bismuth Intoxication

Chronic

GI disturbances,nausea, vomiting

Jaundice

Ulcerative gingivostomatitis,generally with pigmentation

and accompanied by a metallictaste and burning sensation of

the oral mucosa.

Tongue may be sore andinflamed.

Urticaria, exanthematouseruptions , herpes zoster like

eruptions and pigmentation of the

skin and mucous membranes

Acute

Methemoglobin formation

Cyanosis

Dyspnea.

Bismuth pigmentation in the oral


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Bismuth pigmentation in the oral

cavity narrow, bluish-black discoloration of the

gingival margin in areas of preexistent gingivalinflammation.

Such pigmentation results from the precipitationof particles of bismuth sulfide associated withvascular changes in inflammation.

It is not evidence of intoxication but simplyindicates the presence of bismuth in thebloodstream.

Bismuth pigmentation in the oral cavity alsooccurs in cases of intoxication. It assumes a linearform if the marginal gingiva is inflamed.


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Lead Intoxication. Pallor of the face and lips and gastrointestinal symptoms

consisting of nausea, vomiting, loss of appetite, andabdominal colic.

Peripheral neuritis, psychologic disorders, andencephalitis have been reported.

Oral signs- salivation, coated tongue, a peculiar sweetishtaste, gingival pigmentation, and ulceration.

The pigmentation of the gingiva is linear (burtonianline), steel gray, and associated with local irritation.Oral signs may occur without toxic symptoms.


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Mercury Intoxication Headache, insomnia, cardiovascular symptoms, pronounced

salivation (ptyalism), and a metallic taste.

Gingival pigmentation in linear form results from thedeposition of mercuric sulfide.

The chemical also acts as an irritant, which accentuates thepreexistent inflammation and commonly leads to notableulceration of the gingiva and adjacent mucosa and

destruction of the underlying bone.

Mercurial pigmentation of the gingiva also occurs in areas oflocal irritation in patients without symptoms of intoxication.


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TOBACCO USE

V l I B H li


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Vascular

constriction

of the bloodvessels of the

gingiva

Immune

deleteriouseffects onleukocytefunction.

suppress serumantibody levels to

certain periodontalbacteria.

suppressesproduction of theIgG2 both inpatients withperiodontitis andin those withnormalperiodontium.

Directeffects on

tissues

cytotoxicsubstances

can

penetratethe

epitheliumand may

exertdeleteriouseffects on

fibroblasts.

Bone

decreasesintestinal

absorption ofcalcium andmay thereby

affectosteoblast

function andincrease bone

loss inotherwise

healthypostmenopau

sal women.

Healing

Postsurgicalhealing may

beinterferedwith by

absorptionof the toxicsubstancesin tobaccosmoke bythe rootsurfaces.


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1983, Ismail and co-workers analyzed smoking andperiodontal disease and found that smoking remained a majorrisk indicator for periodontal disease after adjusting forpotential confounding variables, such as age, oral hygiene,

and socioeconomic status.

Grossi and co-workers also found a direct and linear doseresponse between level of smoking (pack years) anddestructive periodontitis, supporting the contention thatsmoking is a risk factor for periodontal disease.

Longitudinal studies have confirmed that current smokersexhibited greater disease progression as compared withnonsmokers. Attachment loss is also directly related to serumcotinine levels.


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While there is no evidence that the use of smokeless tobaccoincreases susceptibility to periodontal disease, smokelesstobacco may affect gingival inflammation by affecting levels of

IL-1 and PGE2 in gingival tissues.

Although there is no direct evidence, it is likely that cigar andpipe smoking will have effects similar to cigarette smoking ifthe exposures are comparable.


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CONCLUSION


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sys factors in etiology of pd disease

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