DENTINE HYPERSENSITIVITY

Dr Aghimien osaronseUniversity of Benin School of

Dentistry. Nigeria

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

1. Christian R. Gernhardt. How valid and applicable are current diagnostic criteria and assessment methods for dentin hypersensitivity? An overview. Clin Oral Invest (2013) 17.

2. Mikkilineni M, Rao AS, Tummala M, Elkanti S. Nanodentistry: New buzz in dentistry. Eur J Gen Dent 2013;2:109-13

3. Maryam Moezizadeh Future of dentistry, nanodentistry, ozone therapy and tissue engineering . Journal of Developmental Biology and Tissue Engineering Vol. 5(1), pp. 1-6, April 2013

4. Patrick R. Schmidlin and Phlipp Sahrmann. Current management of dentin hypersensitivity. Clin Oral Investig. 2013 March; 17(Suppl 1): 55–59

5. Rita Chandki et al. ‘NANODENTISTRY’: Exploring the beauty of miniature. J Clin Exp Dent. 2012;4(2):e119-24.

5, Nutalapati R. et al: Nanodentistry – The New Horizon. The Internet Journal of Nanotechnology. 2011 Volume 3 Number 2.

6. Preeti SK et al : A Paradigm Shift-from Fiction to Reality. Journal of undian prosthodontic society , 2011 March; 11(1): 1–6.

7. Sanjay Miglani, Vivek Aggarwal, and Bhoomika Ahuja Dentin hypersensitivity: Recent trends in

management. Journal of Conservative Dentistry 2010 Oct-Dec; 13(4): 218–224

8. Howard E. S, Francis G. S. Dentinal Hypersensitivity: Etiology, Diagnosis and Management. The Academy of Dental Therapeutics and stomatology. 2009

9. Peter Jacobsen et al. Restorative Dentistry An Integrated Approach 2nd Edition. 5: 35-43. 2008

10. José M. R et al. Dentinal sensitivity: Concept and methodology for its objective evaluation. Med Oral Patol Oral Cir Bucal. 2008 Mar1;13(3):E201-6

11. Bartold PM. Dentin hypersensitivity; A review. Australian dental journal 2006; 51:(3):212-218

12. Gillam D.G., R. Orchardson. Advances in the treatment of root dentine sensitivity: mechanisms and treatment principles Endodontic Topics 2006, 13, 13–33

13 Walters PA. Dentinal Hypersensitivity: A Review. Journal of Contemporary Dental Practices 2005 May;(6)2:107-117.

14. Antonio Nanci et al. Oral histology; development, structure and function, 6th Edition. 8:192-240. 1998

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YOU.