Dr. Liya Alice Thomas

First year MDS

CONTENTS• INTRODUCTION• HISTORICAL REVIEW• ETIOLOGY/PREDISPOSING FACTORS• PREVALENCE• THEORIES• CLINICAL FEATURES• METHODS OF EVALUATION• MANAGEMENT• RECENT ADVANCES

INTRODUCTION• Common global oral health problem• Most frequently encountered clinical

problem• One of the oldest recorded complaints of

discomfort• Response to a stimuli varies from person

to person

DEFINITION• “Dentine hypersensitivity is characterized

by short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other form of dental defect or pathology”.

[HOLLAND ET AL,1997]

SO WHAT IS ROOT SENSITIVITY

• PERIODONTAL PERIODONTAL DISEASE TREATMENT

• Different etiology BUT similar pain symptoms

HISTORIC REVIEWYEAR PERSON DISCOVERY

1855 JD WHITE Dentinal pain was caused by movement of fluid in dentinal tubules

1941 LUKOMSKY Advocated sodium fluoride as desensitising agent

1963 BRANNSTROM Hydrodynamic theory of dentinal pain

1986 KLEINBERG Summarised different approaches that are used to treat hypersensitivity

1915 ALFRED GYSI Fluid in the tubule is incompressible

INCIDENCE AND PREVALENCE

• AGE: all age groups

peak incidence : 30-39 yrs

old age : sensitivity because of-

1)secondary & tertiary dentin

2)pulp fibrosis

3)sclerosis of tubules

• SEX : women more frequently affected (15%)

• INTRAORAL DISTRIBUTION: buccal cervical zones of permanent teeth

ETIOLOGY & PREDISPOSING FACTORS

GINGIVAL RECESSION

PRE-DISPOSING FACTORS :-

1)Alveolar bone

2)Tooth anatomy & tooth position

3)Oral hygiene

4)Gingival diseases

5)Trauma

6)Other factors

(1)ANATOMY OF ALVEOLAR BONE :

• Most frequently cited predisposing factor• Thin, fenestrated or absent LABIAL

BONE(Aldritt 1968,Bernimoulan and Curilovie 1977,Lost 1984)

(2)TOOTH ANATOMY & POSITION :

• Tooth anatomy (Olsson and Lindhe 1991) & tooth position (Gorman 1967,Modheer and Odenrick 1980)

can influence alveolar bone thickness

• Orthodontic tooth movement

(3) ORAL HYGIENE :

(4) GINGIVAL DISEASES :

• ANUG

• ANUP

• Chronic periodontitis with associated bone loss can cause recession although the BUCCAL area does not appear to be a site of predilection for periodontal lesions

(5) TRAUMA :

• Non-surgical(scaling & root planing)• Impaction of foreign objects in the

gingiva(Jenkins and Allen 1994)

• Factitious injury(Glenwright and Stranhan 1994)

• Toothbrushing (Sandholm et al 1982 , Bergstrom and Eliasson 1988 , Knocht et al 1993)

(6) OTHER FACTORS :• Frenal pull at the gingival margin

(Mazdyasma and stoner 1980,Powell and McEniery 1981)

• Occlusal trauma (Parfitt and Mjor 1964, Trott and Love 1966)

• Emotional stress (Stone 1948)

NEUROPHYSIOLOGY OF TEETH

• Teeth are supplied by the alveolar branches of the fifth cranial nerve, namely the trigeminal nerve (the maxillary branch in the upper jaw and the mandibular in the lower jaw).

• Pulp is a highly innervated tissue that contains sensory trigeminal afferent axons.

• Sympathetic efferent fibers control the blood flow

• The cell bodies of the sensory neurons of the pulp are located in the trigeminal ganglion. Hundreds, perhaps thousands, of axons enter the pulp through the apical foramen where they branch following the distribution of the blood supply all over the pulp.

• The majority of the nerve bundles reach the coronal dentin where they fan out to form the nerve plexus of Raschkow.

• These then synapse into the odontoblastic cell layer

• Two types of sensory nerve fibres are seen :

Myelinated fibres (A delta{90%} & A beta)

Unmyelinated fibres

A delta fibres – pulp dentin borderin the coronal portion of the pulp & pulp horns

C fibres – core of the pulp

THEORIES OF DENTIN HYPERSENSITIVITY

A number of theories have been proposed over the years to explain the pain mechanism of dentinal hypersensitivity - :

Direct Neural Stimulation

Odontoblast Deformation Theory/Tranducer theory

Hydrodynamic theory

(1)DIRECT NEURAL STIMULATION

• One of the first theories put forth

Drawbacks :

• Nerves are present only in the predentine & inner dentinal zones but donot extend upto the DEJ which is the most sensitive part of the dentine

• Nerves absent in root dentin

(2)Odontoblast Deformation Theory/Tranducer theory

• Rapp et al

Drawbacks :

• Odontoblastic processes extend only partly through the dentin and not upto the DEJ

• No demonstrable neurotransmitters like acetylcholine in the neural transmission of the pulp

(3) Hydrodynamic theory

• Brannstrom• Dentin has over 300,000 tubules/mm2

which is filled with dentinal fluid.• In a vital tooth there is constant slow

outward movement of the fluid through the tubules.

• WIDTH of the tubule is important as the rate of fluid flow is dependent on the fourth power of the radius.

• If tubule diameter doubles a 16 fold increase in fluid flow occurs

• Sensitive teeth have many more(8 times) & wider(2 times)tubules at the buccal cervical area compared to non-sensitive teeth.

• Higher velocity of fluid flow also occurs in tubules with smaller dimeter

• Dentin will only be sensitive if the tubules are patent from pulp to the oral environment & this patency will change with production and removal of the smear layer hence resulting in an episodic condition.

CLINICAL FEATURES –Patients generally complain that pain

arising from dentine hypersensitivity is usually rapid in onset, sharp in character, and short in duration.–Pain is considered to be an

exaggerated response of normal pulp- dentin complex and is only felt on application of external stimulus.–No lingering discomfort once the

stimulus is removed .

DIAGNOSIS

(A) CASE HISTORY :• History & nature of pain• Number & location of the sensitive teeth• Intensity of the pain• Stimuli which initiates the pain• Frequency & duration of sensitivity• Treatment history

(B) CLINICAL EXAMINATION :

• SUbjECTIvE EvALUATION

1. Verbal rating scales

2. Visual analogue scales

3. Verbal descriptor checklists

4. McGill word descriptors

• ObjECTIvE ASSESSmENT

1. Mechanical stimuli

2. Chemical stimulation

3. Electrical stimulation

4. Dehydrating stimulation

5. Thermal stimulation

6. Hydrostatic pressure

SUbjECTIvE EvALUATION

(1)VERBAL RATING SCALES :

• Keele 1948• Four point scale grading pain as SLIGHT ,

MODERATE , SEVERE & AGONIZING• Restrictive choice of words that may not

be very precise with all patients.

(2)VISUAL ANALOGUE SCALES :

• 10cm line.extremes of the line represent limits of pain

• More sensitive in discriminating betwen various treatments and changes in pain intensity

• Best available method

(3)VERBAL DESCRIPTOR CHECKLISTS :

• Allows quantitative assessment of both the sensory and affective dimensions of pain using a continuum across different pain conditions instead of words intended to distinguish conditions (Gracely et al 1978)

(4)McGILL WORD DESCRIPTORS :

• It is used to determine the nature of the discomfort & to monitor response to treatment.

DISADV:reliance on the ability of the subject to understand the words presented to them

ObjECTIvE EvALUATION

(1)MECHANICAL STIMULATION :

(2) CHEMICAL(OSMOTIC) STIMULATION :

• Hypertonic solution of sucrose or calcium chloride (Anderson & Matthews 1967,Clark et al 1987)

• Solute in solution diffuses into the dentinal fluid so on repeated application the osmotic pressure difference between the tubular fluid & applied fluid will decrease & reduce the effect of the solution as an osmotic stimulus(Pashley 1986)

• Long time intervals should be allowed

(3) THERMAL STIMULATION:

(4)DEHYDRATING/EVAPORATIVE STIMULI :

• Combined thermal & evaporative stimulus

• Short air blasts have been recommended to avoid excess evaporation & consequent changes in hypersensitivity (Brannstrom 1963,Pashley et al 1984) & undesirable pulpal effects

• Affects wider area-more intense pain response

(5)ELECTRICAL STIMULATION :

• Quantification of electric current can be used to measure sensitivity

• Determine a condition called PRE-PAIN

• Attributed to larger,more rapidly conducting nerve fibres

• Current applied should be less than 1 milliampere

DIFFERENTIAL DIAGNOSIS• Cracked tooth syndrome(in heavily restored teeth)

• Incorrect placement of dentin adhesives (nanoleakage)

• Fractured restorations• Pulpal response to caries & restorative

treatment• Improperly contoured restorations (traumatic

occlusion)

• Chipped teeth• Vital bleaching

PREVENTION

(1) DIETARY COUNSELLING :

• Reduce dietary acids

(2)TOOTHBRUSHING TECHNIQUES :

(3) PLAQUE CONTROL :

(4)REDUCE OR ELIMINATE

PARAFUNCTIONAL HABITS• Professionally fabricated occlusal

night guards• Re-positioning splints• Stress management

TREATMENT

DESENSITIZATION BY OCCLUDING DENTINAL TUBULES

A)Formation of smear layer

B)Topical agents C)Restorations

1.calcium hydroxide paste D)Lasers 2.calcium phosphate paste

3.silver nitrate

4.strontium chloride

5.fluorides

6.potassium oxalates

7.varnishes

8.dentin adhesives

A) Formation of smear layer :• Isolating the affected tooth &

burnishing the dentin with an orangewood stick.

• Results in the formation of a smear layer which occludes the tubules

• Temporary relief

B) Topical Agents :i)CALCIUM HYDROXIDE –

Mixed with distilled water to form a thick paste

Applied for a few minutes on exposed dentin

Increases remineralizationTemporary relief

ii)CALCIUM PHOSPHATE PASTES –Amorphous calcium phosphate (ACP)Blocks tubules & reduces permeability by 85%

Can also be used to remineralize incipient enamel caries

Commercially available product:GC Tooth Mousse contains ACP & caesin phosphopeptide

iii)SILVER NITRATE –It reduces fluid movement by

precipitating protein or silver chloride within the dentinal tubules.

But it stains dentin and is also damaging to the pulp and gingiva.

Not used anymore

iv)STRONTIUM CHLORIDE –SrCl2 was the first tubule blocking agent to be

introduced into toothpastes

3 MOA :

a)nerve depolarization

b)because it is chemically similar to calcium it can replace lost calcium in hydroxyapatite lattice

c)deposit a layer of fine particles which can occlude the tubules

Commercially available – Sensodyne

Tooth wear & sensitivity – Martin Addy, Graham Embery, W Miachael Edgar & Robin

Orchardson - 1st edition

V)FLUORIDES –Agents like sodium fluoride , stannous

fluoride or acidulated phosphate fluoride may be used for few minutes as mouthrinse, toothpaste or as topical application over exposed dentin.

Act by forming fluoroapatite within tubules which blocks fluid movement within dentin.

STANNOUS FLUORIDEResearch has shown Stannous fluoride to be

effective against dentinal hypersensitivity – 2 to 4 weeks – 0.4% gel

MOA– tin rich surface deposit (in vitro) – nearly complete surface coverage and occlusion of tubules

Topical stannous fluoride – reduces sensitivity on exposed cervical root surfaces

Patricia A. Walters - J Contemp Dent Prac, May 15, 2005, Vol 6, No 2, 107-117

Limitation – potential for temporary extrinsic tooth staining associated with long-term use

Open tubules following treatment After use of SnF2 dentrifice

with non-sensitivity fluoride toothpaste

SODIUM FLUORIDEIncrease in resistance of dentin to acid

decalcification as well as precipitations in exposed dentinal tubules

MOA– precipitated fluoride compounds mechanically blocking exposed dentinal tubules or fluoride within tubules blocking transmission of stimuli

vi)IONOTOPHORESIS -Electrical potential is used to transfer the ions

into the body for therapeutic purposes

METHOD :-Place a negative electrode on the dentin &

positive electrode on the patient’s face/armIsolate teeth with plastic strips or cotton rollsChemical is applied to tooth surface & current is

passed through –ive electrode using 0.5mA current.

Commonly used solutions –

a)30% potassium oxalate

b)6% ferric oxalate

ADV:long term reliefDISADV:1) uses expensive equipment

2)requires more than one application

vii)POTASSIUM OXALATE –Oxalate ions + calcium ions =

calcium oxalate crystals

Very effective method

viii)VARNISHES –Forms a barrier over exposed dentin

& reduces the permeability

Temporary relief

Eg:duraflor,duraphat

ix)DENTIN ADHESIVES-Dentin bonding agents are used Micromechanical bonding through

formation of an interdiffusion hybrid layer

Eg:Gluma desensitizer(Heraeus Kulzer)

Amalgambond(Parkell)

Single Bond(3M)

GLUMA DESENSITIZER

• 5% gluteraldehyde and 35%HEMA in water

• Control DH & decrease post operative sensitvity in restorative procedures

• No mixing & no curing.No repetitive steps.

• No drip formula, so it stays where you place it,minimising contact with soft tissues.

INDICATIONS :• Cervical erosions• Exposed dentin surface• Gingival recession• Under crowns• Bridges• Inlays & onlays• Veneer & temporaries• Margins around temporary crowns• Under all direct restorations.

C)Restorations :• Glass Ionomer Cement or a

Composite Resin Restoration is used

• Long lasting relief

D) Lasers :a.CO2 laser

b.Nd:YAG laser

c. Er:YAG laser

d.He:Ne Laser• MOA- Coagulation & precipitaion of

plasma proteins in the dentinal fluid without altering the surface of dentin.

• A meta-analysis study done by Sgolastra F et al in 2013 proved the efficacy of Nd:YAG over Er:YAG in the treatment of dentinal hypersensitivity.

ADVANTAGES :

i. analgesic

ii. bio-stimulant

iii.anti-inflammatory effects

iv.painless, safe, fast, conservative treatment, and it is well accepted by the patients

DISADVANTAGES

i. High cost

ii. Professional expertise

iii. Thermal side effects

Lasers as a treatment modality for dentinal hypersensitivity-Teresa Mao, Dr. Julie Toby

IOSR Journal of Dental and Medical Sciences (IOSR-JDMS)

e-ISSN: 2279-0853, p-ISSN: 2279-0861. Volume9, Issue2 (Jul.- Aug. 2013), PP 29-32

www.iosrjournals.org

DESENSITIZATION BY BLOCKING PULPAL SENSORY NERVESPOTASSIUM SALTS :• Excitability of intradental nerves• MOA : raise concentration of potassium ions

in the extracellular fluid

Depolarization of nerve cells

Brief excitatory burst

Nerves become unresponsive

• DISADV : works slowly over a period of time

HOW TO USE???

Brushing mouthguard type soft tray

RECENT ADVANCESA. Pro-Argin technology

B. NovaMin

C. Casein Derivatives

A) PRO-ARGIN TECHNOLOGY

• “Saliva based composition” i>Arginine (an aminoacid which is positively

charged at physiological pH)

ii>Bicarbonate (pH buffer)

iii>Calcium carbonate (source of calcium)

• Commercially available as ProClude (instant relief which lasts upto 28days)

• COLGATE has combined ARGININE , CALCIUM CARBONATE & FLUORIDE and this has been clinically proven to provide lasting relief

B) NOVAMIN

• Bioactive glass ceramic material that provides calcium and phosphate

• Calcium sodium phosphosilicate reacts when exposed to aqueous medium to release calcium & phosphate ions which form hydroxy-carbonate apatite

D) CASEIN DERIVATIVES

• Predominant phosphoprotein in BOVINE milk

• In alkaline conditions calcium phosphate is prsent as an alkaline amorphous phase along with casein referred to as casein phosphopeptide-amorphous calcium phosphate

• CPP-ACP : cariostatic agent

USES :

• Preventive therapy in high caries risk patients

• Reduce dental erosion

• Repair enamel involving white spot lesions

• Orthodontic decalcification

• Desensitizing agent

F)CALM-IT DESENSITIZER

• Calm-it™ Desensitizer is glutaraldehyde-based desensitizer that functions by reacting/cross-linking with plasma proteins in dentinal fluid

• Protection for upto 6-months-This simple & effective technique reduces hypersensitivity & eliminates discomfort from cervical erosion.

• Tubule penetration in seconds

• Compatibility with adhesives, cements, restoratives, amalgams, core build-up & temporary materials

G) GLU-SENSE

• The no-drip HEMA/Glutaraldehyde desensitizer that goes where you place it.

• 35%HEMA/5%Glutaraldehyde gel formulation

• acts in seconds to seal dentinal tubules, preventing the fluid shift in them.

• Rub on sensitive area for 30 seconds & allow to dry. Tooth does not need to be completely dry before application. No etching or light curing necessary.Avoid contact with soft tissue.

• Effect lasts 6 months or longer depending on patient. Permanent under restorations.

• Does not interfere with cements or bonding agents

H)GEL-KAM DENTIN BLOCK

• Consists of 0.9% sodium fluoride,0.4% stannous fluoride & 0.14% hydrogen fluoride that can be applied in a tray.

CONCLUSIONScreen patients (does the patient suffer

from stabs of pain or sensitivity)

Obtain patient history

Examine patients to exclude :•Cracked tooth syndrome•Fractured restorations

•Caries•Post operative sensitivity

•Vital bleaching•Traumatic occlusion

No treatment

YESNO

Is your patient’s history consistent with dentin hypersensitivity

Confirm the diagnosis

Initiate management

Follow up

Seek and treat other causes

REFERANCES Textbook of operative dentistry-Vimal K Sikri III edition Clinical Operative Dentistry-Ramya Raghu,Raghu Srinivasan Tooth wear & sensitivity- Martin Addy,Graham Embery,W.

Michael Edgar, Robin Orchardson. Treatment of dentin hypersensitivity-DCNA 2011 Dentin hypersensitivity: Recent Trends in Management- J

CONS DENT, oct-dec 2010 Clinical Dentin Hypersensitivity: Understanding the causes &

prescribing the treatment- Journal of Contemporary Dental Practice.

Dentin hypersensitivity : Etiology,diagnosis and management – A peer-reviewed publication.Howard E Strassler DMD,FADM,FACD and Francis G Serio DMD,MS,MBA,FACD