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Station 1

Station 1
1.1 Bacterial dental plaque ?

Introduction
Dental plaque: a complex biofilm that accumulates on the hard tissues (teeth) in the oral cavity (Marsh, 1995)

Dental Plaque Formation


Glycoproteins from saliva are adsorpted onto the tooth surface

Acquired pellicle

Acquired Pellicle Tooth surface Stage 1: Pellicle formation

Acquired Pellicle Tooth surface Stage 2: Initial Adherence

Acquired Pellicle Tooth surface Stage 4: Maturation

Acquired Pellicle Tooth surface Stage 3: Aggregation

Acquired Pellicle Tooth surface Stage 5: Dispersal

Proteins from saliva and bacteria Acquired pellicle Acquired pellicle

Tooth surface

Plaque formation Formation of acquired pellicle Interaction between early colonizers and the acquired pellicle Coaggregation between the early colonizers and late colonizers Multiplication of adherent cells

Tooth surface

Dental Plaque Formation


Occurs on all surfaces of the teeth and is recognizable clinically within 24 h
Claydon & Addy 1993

It takes 48 h to produce signs of gingival inflammation

Le, 1967

Station 1
1.2 Dental calculus ?

Theories of calculus formation:


Booster mechanisms Epitaxic concept

Theories of calculus formation:


1. Carbon dioxide theory carbon dioxide loss pH

2. pH change by ammonia formation: Urea NH3 pH

Theories of calculus formation:


3. The phosphatase theory:
pyro phosphatase Pyrophosphate supersatureated
Precipitate

4. Seeding theory:
A seeding process calculus

Station 1
1.3 dental plaque calculus
Supragingival plaque / calculus Subgingival plaque / calculus

Supra-subgingival calculus

Dental calculus
Subgingival Harder Coloured (often green) Firmly attached to the tooth Present in smaller deposits, which are not localized near the salivary ducts gingival fluid (serum) origin

Supragingival Friable white yellowish Easily removed by scaling usually recurrent especially in the near the orifices ofmain salivary ducts: Lower incisors Salivary origin

Composition of Supragingival Calculus


Inorganic (~ 80%) Brushite
CaHPO4.2H2O detectable in all deposits after 14 days of development

Organic (~ 20%) Derived from saliva & bacteria


- Largely protein with carbohydrate attached (12-20%) - GAG (CS, HA & HS) from the gingiva -Lipids (3%) perhaps bacterial origin

Octa calcium phosphate Ca8 (HPO4)2 (PO4)4

Wetlockite Ca3 (PO4)2 With some magnesium Instead of calcium Especially in the presence Of fluoride

apatite

Station 2
2.1 2.2 ? 2.3 ? plaque ?

Disclosing agents
Demonstrate presence and location of plaque Evaluation of patient's home-care Erythrosine, fuchsin, fluorescence

Station 3
study cast ( ) plaque

Modifying factor
Local modifying factor
Plaque retention Anatomic predisposing factor Tissue trauma

Systemic modifying factor

Open contact or loose contact

Defective margin of restoration

Poorly designed prosthesis

Station 7
film x-ray ( ) plaque

Station 8
study cast ( ) plaque

Modifying factor
Local modifying factor
Anatomic predisposing factor

Palatogingival groove

Station 9, 10
? ?

PERIODONTIUM
Gingiva Cementum PDL Alveolar bone
Cementum Periodontal ligament Root canal Alveolar bone Apical foramen Alveolar vessels & nerves Pulp cavity Enamel Dentin Gingiva

1 2

3 5 4

1=IDP , 2 = gingival margin , 3 = attached gingiva , 4 = mucogingival junction , 5 = alveolar mucosa

GINGIVA
3 main parts:
Free gingiva Attached gingiva Interdental gingiva

Free gingiva
From gingival margin to the free gingival groove (FGG) at the level of the CEJ. Can be separated form the tooth by a probe Depth of gingival sulcus (crevice) : 0-3 mm.

Free gingiva

Attached gingiva

Extends from the FGG to the mucogingival junction (MGJ)

Attached gingiva
Firmly attached to underlying bone to: withstand masticatory forces withstand forces of tooth brushing prevent movement of marginal gingiva

Attached gingiva

Attached gingiva

Attached gingiva
On the palate, the whole mucosa is keratinised and there is

No MGJ

Keratinized Vs Attached
Attached gingiva Keratinized gingiva FG + AG

KG

Interdental gingiva
Also: interdental papilla Shape determined by:
Contact relationship between teeth width of proximal surfaces shape of the CEJ

Clinical Features of normal (healthy) gingiva


Colour: pink (physiologic/racial pigmentation) Contour: scalloped outline Margins: thin, knife-edge Surface texture: stippled Consistency: resilient Pointed interdental papillae Probing depth: 0-3 mm. No bleeding on probing (BOP).

The gingiva presents a textured surface similar to an orange peel and is referred to as being stippled Stippling varies with age begins to disappear in old age. Stippling

Normal radiographic anatomy of periodontium


Lamina dura (crestal and alveolar) PDL space Interdental septum or Alveolar crest

Periodontal disease
Gingivitis

VS
Periodontitis

Periodontal Disease Periodontal disease


Gingivitis
Limited to the gingival or soft tissues, surrounding the teeth Results in bleeding of gums, and possibly change in color, shape, size, surface texture and consistency Reversible on restoration of hygiene, does not result in destruction of tissues supporting the teeth

Periodontitis
Gingival to the supporting periodontal tissue & destruction of these tissues Irreversible Result in loss of bone supporting the teeth mobility tooth loss

Gingival color

Pale pink

red

hyperpigmentation

Bluished red

Marginal gingiva

Knife edge

round

Stillman s cleft

recession

McCall s festoon

pyramidal

Bulbous/enlargement

edematous

blunt

Interdental papilla
crater

Pocket depth 4 mm.

Gingival recession

Tooth migration

Tooth mobility

Periodontal abscess

Pus discharge and exudation

Bone destruction patterns in periodontitis

Horizontal bone loss

Vertical bone loss or Angular defect

The reference : CEJ to CEJ

Healthy gingiva The gingiva is pale pink in color, knife edge margin , pyramidal IDP, firm in consistency, present of stippling, no bleeding on probing, no gingival recession, no tooth mobility, no pocket formation , no pus and exudate.

Gingival inflammation The gingiva is red in color, round margin , bulbous IDP especially upper and lower anterior teeth, soft in consistency , loss of stippling, bleeding on probing , gingival recession at 23 , 44 ,45 , no tooth mobility , no pocket formation , no pus and exudate.

Systemic

Reference
Thomas G. Wilson, Kenneth S. Kornman., Fundamental of Periodontics, 2nd ed, Quintessence Publishing Co, 2003. Michael G. Newman, Henry H. Takei, Fermin A. Carranza., Clinical Periodontology, 9 th ed, W.B. Saunders company, 2002. Thorkild karring ,Niklaus P.Lang ., Clinical periodontology and Implant dentistry , 3 rd ed.,Munksgaard ,1997. Irving Glickman, Glickman s Clinical Perodontology, 7th ed., W.B. Saunder Co., 1990.

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DHYG 112 Perio I Spring 2008

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Heidi Emmerling, RDH, PhD