CHAPTER SIX

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

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.

B. Gingival (cervicular) fluid provide continuous flushing effect its production and flow increase in relation to the level of inflammation in the gingival tissue. C. Polymorph nuclear neutrophils- is a primary of first line defense in bacterial Plaque develops gingivitis if no treatment formation of pocket results.

Plaque It is a firmly adherent mass of bacterial in muco-polysaccharide matrix. It is the root of most dental and periodontal evils. 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.

Calculus (tartar) Is a calcified deposition found on the teeth and 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.

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

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

2. Periodontitis: - inflammation of deeper structures plus destruction of periodontium, i.e. loss of CT attachment to root surface. - 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.

Histologic progression: 1. Periodontal health: G+ cocci, few spirochetes & motile forms no vasculitis present PMN's and lymphocytes are present as a normal feature Serum proteins and fibrin are contained within the blood vessels the junctional epithelium uniformly joins the CT with rete ridges, the CT is dense and highly organized into tissue fiber bundles

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 JE exudation of fluid from the gingival sulcus increased migration of PMN's into the JE and gingival sulcus loss of perivascular collagen (5-10% of CT may be involved) no visible change.

3. Early lesion (clinically detectable gingivitis): the early lesion appears within 4 - 7 days following the beginning of plaque accumulation lymphoid cells make up 75% of total infiltrate fibroblasts show cytopathic changes possibly associated with interactions with lymphoid cells no apical migration of JE. localized loss of collagen fiber (60 - 70% of collagen fibers are lost in the inflamed area)

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 often appear 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

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.

IV. CLASSIFICATION OF PERIODONTAL DISEASES a. GINGIVITIS 1. Plaque associated gingivitis Most common periodontal disease Clinically characterized by redness, gingival bleeding, edema and enlargement - Overgrowth of gram positive plaque

2. Acute narcotizing ulcerative gingivitis -Acute, recurrent, necrosis of gingival papillae, spontaneous bleeding, pain, and fetor ors. Invasion by spirochetes & fusiforms (Bacteroides intermedius) 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

1) Control of the acute phase

- Broad spectrum antibiotics - Scaling and debridement -mouth washing with antiseptic e.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.

3) Steroid hormone-influenced gingivitis -Manifested by puberty, pregnancy, steroid therapy menstrual cycle associated -Bacteroides enhances with elevated with elevated hormones 4) Medication-influenced gingival overgrowth phenytoin (seizure control), cyclosporin (immunosuppressive therapy, and nifedipine

6) Miscellaneous gingivitis -blood disorders, nutritional deficiencies, tumors, genetic factors, mouthbreathing, diffuse bacterial and viral infections.

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

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 and monocytes. 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

B. Juvenile periodontitis, JP: - characterized by severe angular bone loss in the first molar 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-linked dominant trait. - lack of plaque & clinical inflammation - females 3:1, blacks > whites cont

- good response to curettage and antibiotic treatment. - 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.

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.

C. Pre-pubertal periodontitis: rare condition generalized or localized form - onset after eruption of primary teeth. localized form: - little gingival inflammation. - age 4 or before. - functional defects in either neutrophils or monocytes but not both. - no hx of frequent infections.

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.

3) Refractory periodontitis: - disease in multiple sites with patients demonstrate attachment loss. - any form of periodontitis which does not respond to treatment. - probably an inadequate diagnosis resulting in inadequate therapy. - same organisms as adult perio

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).

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 counts and/or function.

5) Necrotizing Ulcerative Periodontitis: progression of ANUG to include the attachment apparatus

EXAMINATION 2. Assessment methods: clinical : BOP, suppuration, color changes, probing depth changes, 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

 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

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

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.