Dental Biofilm, Soft Deposits, Calculus, and Stain

soft deposits

refers to the acquired pellicle, dental biofilm, material alba, and food debris

dental biofilm

primary risk factor for gingivitis, inflammatory periodontal disease, and dental caries

acquired pellice

definition- a thin tenacious film of proteins, carbohydrates and lipids between the tooth surface and oral environment which can vary in thickness

formation- immediately upon exposure to saliva

functions-

1. regulation of mineral homeostasis

2. host defense and microbial colonization

3. lubrication

removal- with oral self care (formation and maturation can be affected by extrinsic factors)

types of pellicle

Supragingival (don’t see a lot of)- clear and translucent, insoluable (can take on extrinsic stain)

Subgingival- continuous with supragingival pellicle and can be embedded in the tooth surface

dental biofilm and its stages in formation

oral microbiome is dynamic (constantly changing), encapsulated collection of microorganisms

stages:

1. pellicle formation (immediate)

2. initial adhesion (particles floating in mouth)

3. maturation

4. detachment and dispersion (bacteria from big colony detaches & spreads)

composition of dental biofilm

inorganic- calcium, phosphorus, fluoride

organic- polysaccharides (carbohydrates- factor for caries), proteins

• increased acidity —> increased caries risk

changes in biofilm microorganisms

the microbial density is very high and increases as biofilm ages and matures

• more microorganisms—> increased caries and gingivitis

• undisrupted biofilm for 7 days, negative anaerobic bacteria is favored—> increased caries and gingivitis risk—> other inflammatory periodontal diseases increases

• longer bacteria sits—> more pathogenic bacteria (anaerobic)

biofilm days 1-2

gram +, initial layer of subgingival biofilm consists of Actinomyces, streptococci dominates population

biofilm days 2-4

cocci still dominates & multiplies, gram + filamentous form & slender rods, leukocytes

• gradually cocci adhere to filamentous bacteria in a “corn cob” appearance and this is when the bacteria secretes EPS (makes soft plaque thicker and more 3D on tooth)

biofilm days 6-10

• filaments increase in numbers, and a mixed flora appears comprised of rods, filamentous forms, and fusobacteria with heavy accumulations of leukocytes

• gram - anaerobic bacteria such as Porphyromonas gingivalis, spirochetes, and vibrios proliferate (more pathogenic and irritating, deeper in pockets)

• the EPS secreted by the bacteria lead to development of a well-organized three- dimensional structure of the biofilm

biofilm days 10-21

gingivitis clinically evident and seen—> marginal redness

supragingival dental biofilm

• greater variability than subgingival- two layers mainly of gram + aerobic

basal layer- actinomyces

intermediate layer- T. forsythia, F. nucleatum

top later- (spirochetes) P, gingivalis

subgingival dental biofilm

very complex- biome shifts when transitioning from health to disease

• according to picture- epithelium-associated biofilm is more ulcerative and can go into connective tissue and destroy it affecting periodontal ligaments (PDL) which destructs bone!

clinical detection of dental biofilm

• direct vision

• use of explorer and probe

• use of disclosing solution (makes more visible)

• clinical record (document PCR)

biofilm accumulation in protected areas

• areas of crowding

• overhangs, restorations

• distal of most posterior teeth

significance of dental biofilm

plays role in initiation and progression of dental caries and periodontal disease, and significant in formation of dental calculus (mineralized dental biofilm)

dental caries

• microbiome changes

• pH of biofilm is reduced low pH —> more risk!

• fermentable carbohydrates impact bacteria and pH (ex. children eating snacks)

material alba

“cottage cheese”

• soft, white deposit that is clinically visible without disclosing agent

• unorganized collection of living and dead bacteria, desquamated epithelial cells, disintegrating leukocytes, salivary proteins, and food debris

prevention- easily removed with basic mechanical oral self-care

food debris

• after eating, food debris can collect in the cervical third and proximal embrasures

• food impaction can occur, especially in areas of open contacts, diastemas, poorly contoured restorations, or occlusal irregularities

• after it sits (remains), it can contribute to initiation of dental caries and halitosis

location of calculus

supragingival calculus- lingual of sextant 5, buccal of maxillary 1st and 2nd molars

subgingival calculus- generalized or localized apical to gingival margin

calculus composition

inorganic-

• Major = calcium, phosphorus, carbonate, sodium, magnesium

• Trace elements= copper, zinc, etc

• Fluoride in calculus is possible

• Crystals (Brushite (as it sits longer, the crystals change), octocalcium phosphate, hydroxyapatite, whitelockite

organic-

• Various microorganisms, desquamated epithelial cells, leukocytes, and mucin from saliva

• Mineralization of supra- and subgingival calculus essentially the same; source of elements for mineralization is not the same

calculus formation

• factors: genetic, diet (high in carbohydrates—> calculus), malpositioning, etc.

• biofilm is a precursor to calculus formation

• mechanism: saliva & minerals from microorganisms (hard because sits longer)

• types: nodular, thin, ledge

• formation time varies, half of mineralization can begin within 48 hours, mature mineralization approx. 12 days

attachment of calculus

• Attachment by means of an acquired pellicle = easily removed

• Attachment to minute irregularities in the tooth surface by mechanical locking into undercuts (more challenging, interlock together)

• Attachment by direct contact between calcified intercellular matrix and the tooth surface (cementum rough, more difficult)

clinical examination of calculus

supragingival (chalky white) -

• direct examination

• use of compressed air!

subgingival -

• visual examination

• gingival tissue color change

• tactile examination (explorer, currette)

• radiographic examination

• dental endoscopy

prevention of calculus

• personal dental biofilm control (home care)

• regular professional continuing care (scaling)

• anticalculus dentrifice —> tartar control toothpaste (prevents plaque from hardening)

  • pyrophosphate

  • zinc citrate

extrinsic stains

direct extrinsic stain- caused by compounds, organic chromogens (attach to the pellicle —> stain)

indirect extrinsic stain- caused by chemical interaction with tooth surface

frequent stains: yellow (smokers), green, black-line, tobacco (smokers), brown (dietary source- teas, coffee, potential stannous fluoride toothpaste, berries, wine)

less frequent stains: orange and red, metallic

endogenous intrinsic stains

• pulpless or traumatized teeth

  • etiology: pigments from decomposed hemoglobin & pulp discolor dentinal tubules

• disturbances in tooth development

  • hereditary: genetic (amelogenesis/dentinogenesis imperfecta)

  • developmental enamel defects

  • dental fluorosis

• drug-induced stains and discolorations

  • tetracycline- while developing, gray stain (CONTRAINDICATED for children and pregnant women)

  • minocycline (staining post eruption)

exogenous intrinsic stain

• restorative materials

  • silver amalgam (can make tooth look gray)

  • endodontic therapy

• stain in dentin

• other local causes

  • enamel erosion (smoothness- reference picture)

  • attrition (grinding- reference picture)

documentation

documentation related to soft deposits, calculus, and stain should include:

• clinical appearance of teeth relative to deposits

• extent of deposits (slight, moderate, heavy) and location as reference for removal and patient education

• record color, type, extent, and location of stain

• personal patient care procedures demonstrated, preventive measures discussed, and frequency of continuing care appointments

polishing

• polishing paste for stain

• irregular particle shapes will abrade more and polish less

• damage to pulp

bleaching versus whitening

whitening- any process to lighten the tooth color

bleaching- involves free radicals and breakdown of chromogens

vital tooth bleaching

• penetrates enamel & dentin

• each tooth has maximum color change

materials: hydrogen peroxide (quick, works immediately- in office whitening) and carbamide peroxide (slow, longer wear time- at home kits and individuals with sensitive teeth)

• can result in sensitivity and cause burns on gingiva (restorations wont lighten)

  • has irreversible tooth damage- breaks down external surface of tooth, and increase risk for caries!!

• modes: laser (expensive), scalloped and unscalloped (higher risk for chemical burns- not personalized) trays, professionally monitored at-home bleaching tray treatment

breakdown of hydrogen peroxide and carbamide peroxide

carbamide peroxide —> hydrogen peroxide (into oxygen and water) and urea (into ammonia and carbon dioxide)

contraindications for light activated bleaching

• light sensitive people

• people taking a photosensitive medication (lyme’s disease)

• people receiving photochemotherapeutic drugs/tx such as psoralen and UV radiation

indication for tooth bleaching and methods of tx

• discolored, endodontically treated tooth —> internal bleaching: in-office, walking

• single or multiple discolored teeth —> external bleaching: in-office 1-3 visits or custom trays- worn 2-6 weeks

• surface staining —> dental prophylaxis and brushing with whitening toothpaste

• isolated brown or white discoloration, shallow depth in enamel —> microabrasion followed by neutral sodium fluoride applications

• white discoloration on yellowish teeth —> microabrasion followed by custom tray bleaching

dental hygiene process of care

• patient assessment

  • shade guide and spectrophotometer

• dental hygiene diagnosis

• dental hygiene care plan

• implementation

• evaluation and planning for maintenance

fluorosis (too much fluoride)

mild- barely shows changes in enamel

moderate- shows more change in enamel (can get improvement with whitening)

severe- pitted, won’t get whitening back well

documentation

• current oral conditions

• consent to treat related to tooth bleaching

• services provided including necessary records for tooth shade

• impressions and preparation of the trays

• demonstration of tray filling, positioning, timing, and cleaning

• instructions given to patient

• planned follow-up care and appointments

• patient problems or complaints expressed

factors to teach patient

• why a complete oral cancer screening and dental examination, including radiographs and periodontal evaluation, is performed before any form of bleaching is initiated

• during bleaching, teeth and gingival tissues may become sensitive for a time

• if sensitivity is experienced, use a desensitizing product, discontinue bleaching, or delay next treatment

• regardless of method, color relapse occursin a relatively short period of time

• excessive use of bleaching products may be harmful. Follow manufacturer’s directions

• existing tooth-colored restorations will not change color, and therefore may not match and need to be replaced after bleaching