aghimien osaronse
TRANSCRIPT
Aghimien osaronse 20TH SEPT, 2013
DENTIN HYPERSENSITIVITY AND CURRENT TRENDS IN
MANAGEMENT
outline
IntroductionDefinition of dentin hypersensitivity DHSEpidemiologyRelevant anatomy: dentin-pulp complex
Odontoblast and its processes
Dentinal tubules
Sclerosed dentin
Neurovascular bundle Etiopathogenesis
lesion localisation
lesion initiation
Theories of DHS
neural
nerve transduction
hydrodynamicManagement of DHSo diagnosis;
history
examination
differential diagnosis
investigation/tools
definitive diagnosiso prevention/removal of predisposing factors
o Treatment
classification of treatment options
traditional method
current trends in treatment• Arginine-base product Pro-Arginine™• Laser• Bio-glass• Casein phosphopeptide• nanodentistryCONCLUSSIONREFERENCES
introduction
Dentin hypersensitivity is said to be one of most painful and chronic dental condition. Previously described as an enigma because it was poorly understood. It has a higher prevalence among periodontally compromised patients, 60%–98% (Von Troil et al, 2002).
Dentin sensitivity or dentin
hypersensitivity?
Definition
As defined by an international workshop on DH: “Dentine hypersensitivity is characterized by short, sharp pain arising from exposed dentine in response to stimuli, typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other dental defect or pathology”( Holland et al, 1997).
• Dentine Hypersensitivity is a transient tooth pain, characterized by a short, sharp pain arising from exposed dentine in response to a stimulus that cannot be attributed to any other form of dental defect or pathology(Andy M, 2002).
Epidemiology
It occurs in patients 30 to 40 years old, but it can occur in patients significantly younger or older.
female are more commonly affected than males.
Canines and premolars are more affected
OOOCH….
Dentin-pulp complex
The close relation (embryologically, histologically and functionally) between them warrant their discussion as a unit.
Relevant anatomic consideration as it relates to this discussion would be considered. These include;Odontoblast and its processesDentinal tubulesSclerosed dentinNeurovascular bundle
Odontoblast and its processes
They are formed from the ectomesenchymal differentiation of cells of the dental papilla and are responsible for the formation of dentin.
Their processes extend into the dentin.They are more in the coronal dentin than the
root dentinThe processes tend to traverse the entire
length of the tubule
Dentinal tubules
They are channels via which the odontoblastic processes traverse.
They extend the entire length of the dentin permitting diffusion of nutrients through out the dentin
They run a sigmoid shape in the coronal dentin but straight in the root dentin, this is determine by the course of the odontoblast.
Dentinal tubules branch majorly in the root dentin than in coronal dentin.
Dentinal fluid
The odontoblastic processes are surrounded by dentinal fluid inside the tubules.
The dentinal fluid forms around 22% of total volume of dentin.
It is an ultrafiltrate of blood from the pulp via dentinal tubules and forms a communication medium between the pulp (via the odontoblastic layer) and outer regions of the dentin.
Sclerosed dentin
Results from continuous deposition of peritubular
dentin.Mineral deposition within the tubules
without dentin formationmineralisation of the odontoblastic
processes and intra-tubular collagen fibrils.These ultimately reduce permeability of
the dentin thereby prolonging the pulp vitality
Neurovascular supply
A plexus( of Raschkow) of nerve exist in the coronal part of the crown. No plexus exist in the root area as they are supply by ascending branched.
the nerve further extend for a short distance into the dentinal tubules hence, called intra-tubular nerves.
Within the dentinal tubules there are two types of nerve fibers, myelinated (A-fibers) and unmyelinated (C-fibers). The A-fibers are responsible for the sensation of dentinal hypersensitivity, perceived as pain in response to all stimuli.
it is said that the density of the intra-tubular nerve varies as high as one for every two tubules
Etiopathogenesis
Regardless of the cause it is important to state that apart from been expose, the dentinal tubule should be patent for sensitivity to occur.
Two phases are involved in the pathogenesis of dentin hypersensitivity;Lesion localisationLesion initiation
Lesion localisation
This involves the exposure of the dentin a as result of various mechanical or chemical processes;
1. Attrition due to bruxism
2. Erosion
3. Abfraction
4. Abrasion
5. Pocket reduction surgery
6. Tooth preparation for crown
7. Excessive flossing
8. Secondary to periodontal diseases
LESION INITIATION
This involves the actual mechanism that results in the sensitivity felt by the patient. It is on this ground that different theories have been postulated as to how the response is brought about.
1. Direct innervation/neural theory
2. Odontoblastic receptor theory
3. Hydrodynamic/fluid movement theory/Brannstrom 1964
Neural theory
It explains that the nerve is the primary receptor that excites the action potential.
But; Newly erupted teeth are sensitive even when the
plexus of nerves and intra-tubular nerve are not yet establish
Is the outer layer of the dentin directly innervated?
Odontoblastic receptor theory
Odontoblast was postulated as the receptor. It was assume that the odontoblast is of same neural crest origin as the nerve hence, it should retain the ability to transduce and propagate impulses.
But;No organise junction exist between the axon and the
odontoblastic processMembrane potential of the odontoblastic process is too
low to permit transduction
Consistent with the odontoblastic theory are;Odontoblastic process traverse the entire
length of the tubuleThere is the possibility of gap junction
between the odontoblast.
Hydrodynamic theory
Fluid movement within the tubule distort the pulpal environment and is sense by the free nerve ending of the Raschkow plexus. The wider tubules increase the fluid movement and thus the pain response.
The profuse branching of the tubules at the dentin-enamel junction explains the increase sensitivity felt.
The response of pulpal nerves, mainly A delta intra-dentinal afferent fibers, depends upon the pressure applied, i.e. intensity of stimuli.
It has been noted that stimuli which tend to move the fluid away from the pulp–dentine complex produce more pain.
These stimuli include cooling, drying, evaporation and application of hypertonic chemical substances.
Management of DHS
DIAGNOSIS;
HISTORY
EXAMINATION
INVESTIGATION
TREATMENT
TRADITIONAL METHOD
CURRENT TRENDS IN TREATMENT
IMPORTANT STEPS TO FOLLOW
1. Correct diagnosis of dentin hypersensitivity including a patient’s history screening and a brief clinical examination
2. Identification of etiologic and predisposing factors
3. Differential diagnosis, to exclude all other dental conditions
4. If present, treatment of all conditions with symptoms similar to dentin hypersensitivity
5. Removal or minimization of etiologic and predisposing factors
history
Occur in females than males; this is in keeping with their dietary practices
Middle age group of 30-40 years are commonly affected
Pain is described as sharp, short lasting irrespective of the stimuli and usually of chronic duration History of excessive tooth brushing, flossing and oral habit should be checked.
Past dental treatment like vital tooth bleaching, periodontal procedures 54%–55% (Howard E. S, 2009).
Medical condition that results in tooth wear lesion bulemics and gastrointestinal reflux disease
Social practices involving intake of acidic foods and drinks(quantity and frequency)
EXAMINATION
Evidence of tooth wear lesion (attrition, abrasion, erosion)
Gingival recession
Exposed root surfaces
Recession and attrition
investigations
• It is important to note that DHS is a diagnosis of exclusion hence, effort should be made to rule out other conditions that would mimic this presentation. The following diagnostic tools could help;
1. Air jet
2. Cold water jet
3. Electrical devices
4. Dental explorer
5. Periodontal probe
6. Radiographs
7. Caries diagnostic devices
8. Percussion testing
9. Assessment of occlusion
10. Bite stress tests
Differentials
Bite stress test, transillumination could help diagnosis a fracture
Percussion test could exclude pulpitis and periodontal involvement
Radiographs or other caries detecting devices exclude caries(root)
Occlusion assessment could rule out traumatic occlusion from high restoration
Differential diagnosis
Cracked tooth syndromeFractured restorationsRestorations left in traumatic occlusionChipped teethDental caries, root cariesPostoperative sensitivityPulpal response to restorative treatment or
certain materialsMarginal leakage of restorationsPulpitis, pulpal statusVital bleaching procedures
Definitive diagnosis
A simple clinical method of diagnosing DHS includes a jet of air or using an exploratory probe on the exposed dentin, in a mesio-distal direction,
Prevention/eliminate predisposing factors
1) Ensure proper toothbrush consistency, ensure proper brushing technique, highly abrasive tooth powder or pastes should be avoided.
2) Avoid over-brushing with excessive pressure or for an extended period of time or excessive flossing
3) Avoid brushing immediately after taking acidic drinks
4) Avoid over-polishing exposed dentin during stain removal.
Prevention cont’d
5) Avoid over-instrumenting the root surfaces during scaling and root planing, particularly in the cervical area of the tooth.
6) Avoid violating the biologic width during restoration placement, as this may cause recession.
7) Patient with gastrointestinal reflux disease should be properly managed by the physician and fabrication of occlusal splint to cover the affected areas, to prevent their contact with the acids.
Treatment of DHS
• Classification of treatment options• Ideal properties of a desensitizing
agent• Traditional methods of treatment• Current trends in treatment
Two main group of products are available;To occlude or plug the tubulesNerve desensitisers
CLASSIFICATION OF DESENSITIZING AGENTS
1. Base on mode of administration:
at-home
in-office
2. Base on mode of action
Nerve desensitization
Protein precipitation
Plugging dentinal tubules
Dentine adhesive sealers
Lasers
Homeopathic medication
3.’’ Others’’
gingival graft
1. Mode of administration
At home desensitizing agents
In-office treatment
2. On the basis of mechanism of action
A. Nerve desensitization
Potassium nitrate
B. Protein precipitation
Gluteraldehyde
Silver nitrate
Zinc chloride
Strontium chloride hexahydrate
C. Plugging dentinal tubules
STROTIUM ACETATE…..SENSODYNE RAPID ACTION
Sodium fluoride
Stannous fluoride
Potassium oxalate
Calcium phosphate
Calcium carbonate
Bio active glasses (SiO –P O –CaO–Na O)
D. Dentine adhesive sealers
Fluoride varnishes
Oxalic acid and resin
Glass ionomer cements
Composites
Dentin bonding agents
E. Periodontal soft tissue grafting.
F. Anti-inflammatory
corticosteroids
G. Crown placement and restorative materials
H. Lasers Neodymium:yttrium aluminum garnet (Nd-
YAG) laser GaAlAs (galium-aluminium-arsenide laser) Erbium-YAG laser He:Ne laser
I. Homeopathic medication
Propolis
Ideal properties of a desensitizing agent
(Grossman et al, 1965)
1. Rapidly acting with long-term effects,
2. non-irritant to pulp,
3. painless
4. easy to apply, and
5. Should not stain the tooth.
Traditional treatment methods
A. Adhesive composite resin, GIC and dentin bonding agents;
Indicated when the exposed sensitive root surface has surface loss due to abrasion, erosion and/or abfraction leaving a notching of the root.
The adhesive resins can seal the dentinal tubules effectively by forming a hybrid layer.
Newer bonding agents modify the smear layer and incorporate it into the hybrid layer.
Hydroxyethyl methacrylate (HEMA), forms deep resinous tags and occludes the dentinal tubules. 5% of Gluteraldehyde
could be added to 35% of HEMA causing coagulation of the proteins inside the
dentinal tubules
B. Fluoride varnish:(e.g. sodium fluoride, stannous fluoride)
Fluorides decrease the dentinal permeability by precipitation of calcium fluoride crystals inside the dentinal tubules.
5% sodium fluoride varnish painted over exposed root surfaces is effective treatment of DHS.
C. oxalate. precipitates and occlude the open dentinal
tubules. Oxalate reacts with the calcium ions of dentine
and forms calcium oxalate crystals inside the dentinal tubules as well as on the dentinal surface.
Topical application of 3% potassium oxalate can reduce DHS post periodontal surgery.
Avoid using with tray for a long time as it can cause gastric irritation.
D. desensitizing dentifrices. desensitizing ingredient in toothpastes is potassium
nitrate. It acts by penetrating the A-fibres of the nerves
reducing its excitabilty. for a potassium nitrate toothpaste it must contain
5% potassium nitrate. It takes up to two weeks to show any effectiveness
Others.
Gingival graft;
This is indicated when recession is progressive, aesthetic is a major concern and when the treatment is not responding to convention treatment, including coronally reposition flaps, lateral sliding graft, free gingival and connective tissue graft
Anti-inflammatory
Topical application 0.5% solution of prednisolone on exposed root surface will induce remineralisation leading to tubular occlusion.
Fluoride Iontophoresis can also be used, a technique that utilizes a low galvanic current to accelerate ionic exchanges and precipitation of insoluble calcium with fluoride gels to occlude the open tubules.
Current trends in treatment of DHS
a. Arginine-base product Pro-Arginine™
b. Laser
c. Bio-glass
d. Casein phosphopeptide
e. nanodentistry
Arginine-base product
Utilizes arginine, an amino acid; bicarbonate, a pH buffer; and calcium carbonate, a source of calcium.
Mechanism of action is based upon the role that saliva plays in naturally reducing dentinal hypersensitivity
Arginine at a neutral pH is positively charged and bind to the negatively charged tubules thereby attracting a calcium-rich layer from the saliva to infiltrate and block the dentinal tubules.
The dentin plug contained high amounts of phosphate, calcium and carbonate and also significantly reduced the flow of dentinal fluid in the tubules.
A slow speed hand piece is use to apply the paste on the exposed tubule.
It provides instant relief from discomfort that lasted 4 weeks after a single application with 71.7% reduction in sensitivity measured by air-blast and an 84.2% reduction by the “scratch” test immediately following application (Kleinberg I.S, 2002).
Significant relieve is experienced when applied before dental procedure.
Occlusion of dentinal tubules by the Pro-Argin™
technology
Laser
MECHANISM OF ACTION
a. Occlusion of dentinal tubules e.g. Nd-YAG
b. Alteration of nerve transmission. GaAlAs
c. Coagulation of proteins within the dentinal tubules and blockage of fluid movement.
d. deposition of insoluble salts into the exposed dentinal tubules: Er: YAG laser
LASER can be carried out alone or in association with surface treatment.
Casein phosphopeptide–amorphous calcium phosphate
CCP- ACP
The phosphoseryl sequences within the casein phosphopeptide get attached to the ACP which maintain a supersaturated solution of bioavailable calcium and phosphates.
The stabilised CCP-ACP is able to remineralised subsurface enamel lesion which is also important in treatment of dentine sensitivity.
ACP can be used to control bleaching sensitivity when incorporated into bleaching gels.
Direct application on teeth by brushing could relieve sensitivity.
Bioglass (NovaMin)
e.g. calcium sodium phosphosilicate bioactive glass e.g. NovaMinR
Has silica as the main component, acting as a nucleation site for the precipitation of calcium and phosphate.
Upon its application an apatite layer is formed which occlude the tubule.
Relieve should be expected after 6 weeks of home used.
THE PLACE OF NANODENTISTRY
Nanodentistry will make possible the maintenance of comprehensive oral health by employing nanomaterials, biotechnology, including tissue engineering, and ultimately dental nanorobotics(robots at the nanoscale.).
These nanorobots will be able to bring about a variety of functions as they exert precise control over matter.
In the area dentine sensitivity nanorobots could selectively and precisely occlude selected tubules in minutes, offering patients a quick and permanent cure (Mallanagouda et al., 2008; Jhaver, 2005; Freitas, 2005).
isn’t this wonderful?
Dentin hypersensitivity is always a diagnosis of exclusion, it is confirmed only after all possible other conditions have been diagnostically eliminated
The importance of implementing preventative strategies in identifying and eliminating predisposing factors in particularly erosive factors (e.g. dietary acids) cannot be ignored if you as the practitioner is going to treat this troublesome, stubborn and recalcitrant clinical condition successfully.
Conclusion
Depending on the severity of dentinal hypersensitivity, clinical management may include both in-office and self-applied at-home therapies, including recent and novel technologies that have been introduced.
The least invasive, most cost-effective treatment is the use of an effective desensitizing toothpaste.
references
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GENTLEMEN AND LADIES…THANK
YOU.