Gingival Recession and Dentine Hypersensitivity Flashcards
Define Gingival Recession?
Gingival recession is defined as an apical shift of the gingival margin, causing exposure of the root surface of a tooth. Location of the marginal tissue apical to the cemento - enamel junction with exposure of the root surface
New classification scheme for periodontal and peri-implant diseases and conditions (2018):
Other Conditions Affecting the Periodontium-Mucogingival Deformities and Conditions-
Mucogingival deformities and conditions around teeth
Gingival phenotype Gingival / soft tissue recession Lack of gingiva Decreased vestibular depth Aberrant frenum / muscle position Gingival excess Abnormal colour Condition of the exposed root surface
Prevalence:
Recession of 1mm or more in 58% of adults age 30+
Increased prevalence and extent with age
37.8% and extent of 8.6% of teeth in 30-39 year olds
90.4% and extent of 56.3% in 80-90 year olds
Greater gingival recession:
Left side of jaw
Males V females
Afrocarribeans V white Caucasians
Aetiology of recession:
Bone morphology- Crestal bone Trauma Keratinised Tissue Local Plaque Retention Factors restorative dentistry calculus and plaque Malocclusion High attachment of fraenum Periodontal disease
Bone morphology- Crestal bone
Tooth positioning in the arch can affect the bone morphology around a tooth, gingival recession comes with alveolar bone dehiscence, it is not clear whether this develops before gingival recession or in parallel
Trauma
Foreign bodies: Lower lip piercing/ Finger nail picking
Toothbrushing: Hard toothbrush, frequency, frequency of changing brush, technique
Partial dentures: Poorly designed or maintained/ Oral hygiene
Chemical trauma: Topical cocaine
Keratinised Tissue
It was believed that a certain apico-coronal width of keratinised tissue was required, No minimum width.
Thickness and texture of attached gingiva is important,
thin, fragile tissue pre-disposed to recession in presence of plaque-induced inflammation or trauma
Local Plaque Retention Factors
High muscle attachment and frenal pull
Restorative dentistry:
subgingival margins increase plaque retention
more pronounced inflammation seen in thin gingiva
? Does increase in thickness decrease risk of recession
calculus/plaque: studies correlate the prevalence of generalised recession with high levels of batcerial deposits round the tooth
Periodontal disease
pocket redcuing following successful NSPT, surgical trratment may also result in more gingiva; recession
Clinical Outcome of gingival recession:
Dentine Hypersensitivity Aesthetic concerns Plaque retention and inflammtion tooth abrasion root caries
Define dentine hypersensitivty:
Dentine hypersensitivity is characterised by short, sharp pain arising from exposed dentine in response to certain stimuli, which cannot be attributed to any other dental defect or disease
It may go on to manifest as a dull ache beyond the duration of the stimulus, possibly as an altered (irreversible) pulpal response
Epidemiology of dentine hypersensitivity:
Peak incidence is 20-40 years
Gender bias to sensitivity, F>M
And at an earlier age
Could be due to better OH, F>M
Distribution of dentine hypersensitivity
Most frequently the buccal/labial cervical areas of teeth In order of most often affected teeth First premolars Canines Incisors Second premolars Molars Correspond to areas of gingival recession Correspond to areas of thinning enamel Correspond to areas of cementum loss
Types of stumli :
Thermal- hot and cold
Osmotic (hypertonic solutions)
Sweet/ Spicy/ Acid
Micro-organisms and their metabolites can penetrate tubules (?)
Desiccation-Drying of lesions often stimulates pain
With evaporation of fluids, there may be a thermal element
Electrical -Galvanic reactionsElectric pulp testing
Tactil-Touching/Probing/Tooth brushing
Mechanism of sensitivity conduction
Odontoblasts as receptors?
Inconclusive
Nerves in dentine?
Only seen in 1% of tubules in the cervical margin, however electrical current and cold stimulate nerves directly
Hydrodynamic mechanism?
Currently accepted hypothesis (Brännström, 1963)
Brännström hydrodynamic hypothesis
Dentine hypersensitivity caused by the movement of dentinal tubule contents
Increased outward fluid flow causes a pressure change across the dentine
Distortion of A-delta fibre causes pain
Brännström hydrodynamic hypothesis
Dentine hypersensitivity caused by the movement of dentinal tubule contents
Increased outward fluid flow causes a pressure change across the dentine
Distortion of A-delta fibre causes pain
May be another process involved
Fluid flow changes also result in an electrical discharge
This may be able to stimulate nerves electrically
why does size matter?
Width of tubule
Rate of fluid flow depends on 4th power of the radius
So if a tubule is twice the width fluid flow is 16 times greater
Sensitive dentine shows:
A disrupted smear layer
Many more dentinal tubules at the surface
Tubules not occluded by deposits
Tubule diameter wider
Root sensitivity
Term proposed for dentine hypersensitivity from gingival recession due to periodontal disease and treatment
Potentially microorganisms invading root dentinal tubules. May be different aetiology
Dentine Exposure
Resulting from loss of enamel
Removal of enamel by restorative procedures
Attrition (not in cervical buccal lesions)
Abrasion
Erosion
Combined erosion and abrasion
The role of Toothbrushing
Tooth brushing alone has no significant effect on hard tissues
Plus toothpaste, has potential to abrade dentine considerably
Toothbrush design/bristles may contribute indirectly
The role of toothpaste
Abrasive particles might remove the smear layer and open tubules
Detergents might help to remove the smear layer
Tubules could be occluded with particulate matter from the paste
Erosion
Intrinsic or extrinsic source of acids
enamel and dentine loss and surface softening
tooth surface loss by toothpaste abrasion if intra-oral environment acid
what factors other then PH in progression of erosion?
pH of the acid is not the only factor in erosion
Type, chemical strength, temperature, exposure time are other variables
Think of fruits other than citrus, health supplements, mouthwashes, fruit teas, alcopops, wine etc.
History, examination and diagnosis?
Record extent of recession (millers classification)
Descriptive
Index
Identify aetiological factors
Classically, dentine hypersensitivity is:
Of a sharp nature, duration usually as long as stimulus
Main stimuli cold or evaporative
Differential diagnosis for dentine hypersensitivity
Cracked tooth syndrome Incorrect placement of dentine bonding agents Fractured restorations Pulpal response to caries and restorative treatment Restoration left high in occlusion Palatogingival groove Chipped tooth Vital bleaching
TReatment planning?
Pain management
Prevent progression
Periodontal screening and early treatment
Managing hypersensitivity
Tubule occlusion
Blocking pulpal nerve response
Tubule occlusion
promotes formation of new tissue eg: smear layer, intratubular dentine, tertiary dentine in response to stimulus or trauma
application of an artificial barrier e.g.: varnish, dentine bonding agents, composite resins, GIC and toothpastes
Blocking pulpal nerve response
Potassium ions diffuse along tubules and raise extracellular K+ conc, reducing nerve excitability
Unproven in humans
Clinically unlikely that ions will diffuse into tubules against flow of dentinal fluid
Ideal qualities of barrier materials
Retentive Insoluble Penetrate tubules Form mechanical tags into tubules Seal the end of tubules
Managing hypersensitivity: home use products
Toothpastes, gels and mouthwashes
Contain potassium, strontium, oxalate and fluoride salts
Potassium nitrate: Cochrane review (2005) no clear evidence
Novamin: releases of calcium and phosphate ions from saliva to give a hydroxyapatite-like layer
Long term use needed (cumulative dosing for effect)
The placebo effect
All products achieved a modest reduction in hypersensitivity
This was irrespective of presence of active ingredients
West et al (1997) showed a placebo effect of 40%
Managing hypersensitivity: in-surgery products
Varnish eg. Duraphat (5% NaF), Clinpro (5% NaF & Tricalcium phosphate)
1-3 layers of adhesive resin bonding systems eg. Seal and Protect, Optibond Solo, Scotchbond 1 (+ etchant?)
Desensitising polishing paste (calcium carbonate and arginine)
Reinforced GIC where there is abrasion cavity progression
Watch for overhangs at the gingival margin
Comparison of efficacy
Fluoride varnish
Reasonable efficacy but dissolution over time
Resins
Good if film thickness adequate. Products which do not require etching (Ide et al. 1998)
GIC
Good at occluding tubules where indicated for use
Preventive Patient Advice
Oral hygiene advice Change from damaging brushing techniques to: Modified Bass technique Roll technique Electric toothbrushes Smoking cessation Traumatic habits Reduce risk factors Diet history Limit acidic drinks, do not brush immediately after Night-time splints if wear from bruxism
