perio six.ppt

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Periodontal disease

Anatomical consideration-normal gingiva is

pink, firm with well formed papillae

and gingival crevices.

Parts of the normal gingival

Free gingiva (inter-dental papillae)

Attached gingival

Alveolar mucosa

CHAPTER SIX


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Deffence mechanism of the oral cavity

This includes saliva , cervicular (gingival)

fluid, polymorph nuclear leukocytes and

certain micro-organisms.

A. Saliva-flushing action

it contain the secretors immunoglobulin IgA,agglutins, lysozyme, lactoferrin Which

interferes with bacterial adhesion and growth.


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B. Gingival (cervicular) fluid provide continuousflushing effect

its production and flow increase in relation

to the level of inflammation in the gingivaltissue.

C. Polymorph nuclear neutrophils- is a primary

of first line defense in bacterial Plaque develops gingivitis if no treatment formation

of pocket results.


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Plaque

It is a firmly adherent mass of bacterial inmuco-polysaccharide matrix.

It is the root of most dental and periodontalevils.

Clinically it is difficult to identify with necked

eye at initial stages. When the deposition reached at a certain

thickness can it be seen as yellowish.


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Calculus (tartar)

Is a calcified deposition found on the teethand is formed by mineralization of plaque

deposits. Location-mostly found opposite the opening

of the salivary ducts.

e.g stensens duct- maxillary molar area.Whartons duct-lingual area of lower

anterior tooth.


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Periodontum

It is supporting apparatus of the teeth. It

includes:

The gingiva (free, attached and alveolar mucosa)

Alveolar bone

Periodontal ligament

Cementum

Blood vessel of the area


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INFLAMMATION:

1. Gingivitis:

- inflammation of gingiva soft tissues (onset any

age).

- gingival bleeding, color change to red or purple

- gingival pseudopockets may develop,

- may or may not progress to periodontitis

- reversible generally present with periodontitis


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2. Periodontitis:

- inflammation of deeper structures plus destruction ofperiodontium, i.e. loss of CT attachment to rootsurface.

- loss of bone adjacent to that area. - then replacement of CT attaches to root surface by JE.

- apical migration of JE.

- coronal aspect of JE breaks down resulting in pocket

formation. - degeneration of CT attachment occurs before pocket

formation.


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Histologic progression:

1. Periodontal health:

G+ cocci, few spirochetes & motile forms

no vasculitis present

PMN's and lymphocytes are present as a normalfeature

Serum proteins and fibrin are contained within theblood vessels

the junctional epithelium uniformly joins the CT withrete ridges, the CT is dense

and highly organized into tissue fiber bundles


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2. Initial lesion (subclinical gingivitis):

Starts with health and take away oral hygiene.

In 2-4 days get perivascular infiltrate of PMN's in JE.

vasculitis of vessels adjacent to JEexudation of fluid from the gingival sulcus

increased migration of PMN's into the JE and gingivalsulcus

loss of perivascular collagen (5-10% of CT may beinvolved)

no visible change.


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3. Early lesion (clinically detectable gingivitis):

the early lesion appears within 4 - 7 daysfollowing the beginning of plaque accumulation

lymphoid cells make up 75% of total infiltratefibroblasts show cytopathic changes possibly

associated with interactions with lymphoid cells

no apical migration of JE.

localized loss of collagen fiber (60 -70% ofcollagen fibers are lost in the inflamed area)


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4. Established lesion (severe gingivitis):

develops within 2-3 weeks

may still be reversible as gingivitis

acute inflammation

may progress to advanced lesion but more oftenappear not to progress.

lesion dominated by plasma cells.

May/ may not have gingival pocket - coronal part of JE

breaks down. - apical part of JE intact.

continued loss of collagen and CT substance


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5. Advanced lesion (periodontitis):

develops in years to decades

formation of periodontal pockets.

plasma cells dominate lesion.

continued loss of collagen subjacent to the pocket epithelium

extension of the lesion into alveolar bone and PDL with

significant bone loss

permanent destruction of deeper structures.

loss of attachment formation of periodontal pockets

< 50% of population progress to advanced lesion. periodontitis.


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IV. CLASSIFICATION OF PERIODONTAL

DISEASES

a. GINGIVITIS

1. Plaque associated gingivitis

Most common periodontal disease

Clinically characterized by redness, gingivalbleeding, edema and enlargement

- Overgrowth of gram positive plaque


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2. Acute narcotizing ulcerative gingivitis

-Acute, recurrent, necrosis of gingival papillae, spontaneous bleeding, pain,and fetor ors. Invasion by spirochetes & fusiforms (Bacteroidesintermedius)

Clinical features

- inter proximal ulcer- Necrosis of papillae (free gingival)

- Pain

- Easily bleeding

- Foetor oris

- Lymphadenitis

- Fever and malaise

Treatment 1) control of the acute phase

2) Management of the residual condition


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1) Control of the acute phase

- Broad spectrum antibiotics

- Scaling and debridement

-mouth washing with antiseptice.g. chlorohexidine 0.2%

2) Management of the residual condition

- Supra and sub gingival scaling

- Root planning and gigivoplasty

NB. Patient with recurrence should undergo medical

examination and screening for HIV.


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3) Steroid hormone-influenced gingivitis

-Manifested by puberty, pregnancy, steroid

therapy menstrual cycle associated

-Bacteroides enhances with elevatedwith

elevated hormones

4) Medication-influenced gingival overgrowth

phenytoin (seizure control), cyclosporin

(immunosuppressive therapy, and nifedipine


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6) Miscellaneous gingivitis

-blood disorders, nutritional deficiencies,

tumors, genetic factors, mouthbreathing,

diffuse bacterial and viral infections.


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b. PERIODONTITIS:

1) Adult periodontitis:

- most common form, plaque & calculus -related.

- onset in adolescence and continues for the life of individual.

- prevalence and severity increases with age, with no sex

predilection

- usually horizontal bone loss.

- blood cell defects not commonly found. - Bacteria vary (attached)Actinomyces israelii, A. naeslundii,

and A. viscosus

- Unattached portion of subgingival plaque is spirochetes &

gram (-) rods


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2) Early Onset Periodontitis

A. Rapidly progressive periodontitis:

Type A = younger, little plaque, neutrophil problems

- severe gingival inflammation & rapid lose of CTA & alveolar

bone support. - onset = young adults puberty to age 35.

- 66% have depressed neutrophils chemotaxis response andmonocytes.

Type B = 26-35 years, significant plaque & calculus, OK

neutrophils - Acute phase may have associated malaise, weight loss and

depression.

- Can respond well to scaling and antibiotic therapy

- RPP related to: diabetes mellitus type I, Downs

syndrome,and AIDS


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B. Juvenile periodontitis, JP:

- characterized by severe angular bone loss in the firstmolar in otherwise healthy

adolescents. Lesions are often bilaterally symmetrical. (3-5X

adult rate of loss) - permanent 1st molars and sometimes incisors, usually

bilaterally symmetrical

- My have genetic basis, and be inherited as an X-linkeddominant trait.

- lack of plaque & clinical inflammation - females 3:1, blacks > whites

cont


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- good response to curettage and antibiotictreatment.

- tetracycline 1gram/day 14-21 days

before meals and at bedtime.Bacteria: Haemophilus (Actinobacillus)actinomycetemcomitans, B intermedius ,

A.A.- gram (-) rod, non-motile, inhibits PMN

chemotaxis.- capnocytophaga- gram (-) rod.

- Prevotella- gram (-) rod, non-motile.


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Localized, LJP:

- vertical bone loss 1st molars.

- horizontal bone loss incisors.

- mirror image defects 75% bilateral symmetry, furcations

intact. - peripheral PMN's defective 75% of cases.

Generalized, GJP:

- horizontal bone loss.

- may be same as rapidly progressive p.

- post juvenile periodontitis:

- dramatic decrease in rate of destruction

- affected sites clinically similar to adult p.


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C. Pre-pubertal periodontitis: rare conditiongeneralized or localized form

- onset after eruption of primary teeth.

localized form:- little gingival inflammation.

- age 4 or before.

- functional defects in either neutrophils ormonocytes but not both.

- no hx of frequent infections.


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Generalized form:

- acute, red, proliferative gingival inflammation.

- rapid destruction.

- peripheral WBC's increased.

- PMN defects, absent from gingival tissues.

- frequent infections, otitis media, skin, URI.

- refractory to antibiotic therapy.

- primary & secondary teeth affected.


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4) Periodontitis associated with systemic disease

- HIV associated periodontitis

- rapid onset and progressive p.

- 6-12 mm bone loss .

- interproximal necrosis and cratering. - marked edema and intense erythema of gingiva.

- acute pain and spontaneous bleeding.

Treatment:

- scale and root planning. - OHI.

- metronidazole 500 mg tid (7 days).


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Systemic diseases predispose to periodontitis:

- insulin dependent diabetes mellitus, IDDM.

- Down's syndrome.

- early in life, doubtful infective origin, mimics JP.- Crohn's disease

- neutropenia

- agranulocytosis

- leukemia

all have in common defective neutrophil countsand/or function.


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5) Necrotizing Ulcerative Periodontitis:

progression of ANUG to include the

attachment apparatus


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EXAMINATION

2. Assessment methods:

clinical : BOP, suppuration, color changes, probing depthchanges, attachment level changes, gingival crevicular fluid

flow, temperature probe microbiological = culture and sensitivity DNA probe

(species specific DNA, limited to 3 species;AA, P. gingivalis& P.intermedius, phase contrast microscopy (spirochetes &motile), Gram stain (morphology)

immunological = PMNs, lymphocytes, antibody titers,complement fractions, lymphokines

- enzyme analysis


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Organisms associated with different tissue

conditions:

- healthy sulcus, gram (+) predominate.

- gingivitis, shift to gram (-).

- adult periodontitis, gram (-) anaerobic rods,

30-50% motile rods and spirochetes.

- JP, Gram (-)A.A., P. gingivalis, P.

melaninogenicus & Porphyromonas


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Clinical methods of direct observation:

- subgingival plaque and calculus.

- gingival inflammation.

- bleeding on probing (BOP).

- suppuration.

- loss of form.

- gingival retraction.

- pocket depth/probing depths


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Treatment plan:

a] non-surgical:

- laboratory test, medical/dental consults.

- eliminate pain/infection, address chief complaint.

- remove etiological factors by mechanical means. - increase oral hygiene.

- caries control, endo, extractions, occlusal adj.

- antimicrobial therapy.

- peridex, hydrogen peroxide - evaluation of oral hygiene.

- evaluation of response to factors listed above.


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