PATHOPHYSIOLOGY OF:

TOOTH ACHE

Trianggoro Budisulistyo
trianggoro.b@gmail.com

Dept of Neurology Diponegoro University/ Dr. Kariadi Hospital

Sensory Receptors
■ MONITORING; capturing internal and external
environment alteration
■ TRANSMITTING; continuing the nerves impulse from
peripheral to CNS
■ ALERTING; critical of homeostasis pathological events

CONTINUALLY PROVIDE US WITH INFORMATION OF

SURROUNDING CHANGES
 Sensory Receptors: Functional
■ CHEMORECEPTORS
– Respond to chemical concentration altered
■ MECHANORECEPTORS
– Respond to mechanical stimuli: touch, pressure, vibration
■ PHOTORECEPTORS
– Respond to light stimulus
■ THERMORECEPTORS
– Respond to temperature changes
■ NOCICEPTORS
– Respond to tissue(s) damage causing pain
Classification of Sensory Input
■ SOMATHESTETIC SENSES
– Sensors lied in the whole body area:TOUCH,
PRESSURE, LIMB MOVEMENTS, PAIN, HEAT & COLD
– Information usually conducted to the spinal cord
first then transmitted to the brain
■ SPECIAL SENSES
– Changes detected only by specialized sense organs
in the head: SMELL, TASTE, HEARING, VISION,
EQUILIBRIUM
– Information conducted directly to the brain
 Disorders of Sensory Systems
■ Reduced
– Disorders of sense organs or receptors
– Afferent nerves lession
– Eg. Hipesthesia-anesthesia, Visual impairment,Hearing loss, etc
■ Increased
– Physical stimuli sensation alteration
– Sensation without stimuli
– Hyperalgesia, Tingling, Tinnitus, Central Neuropathic Pain
■ Incorrect Responses
– Allodynia, Hyperpathia, Hyperacusis, etc
 What is Pain?
■Pain is part of the body's
defense system.
■The reflex reaction to escape
painful stimulus is meant to
adjust behavior to avoid the
harmful situation in the future.
■PAIN is an unpleasant sensory &
emotional experience associated with
actual or potential tissue damage or
described in terms of such damage
 True for Acute Pain which is our friend = a
disease itself
 Chronic Pain is a false alarm
– Persistant more than 6 months
-Not amenable to routine pain control methods
-Exists beyond an expected time frame for
healing
-Healing process may never occur

Boswell MV, et al. Pain Physician Vol. 8, No. 1, 2005

 COLDSPA Memory Guide
■ Character: Describe the pain. How does it feel? Be specific. Is it
constant, occasional, or recurring?
■ Onset: When did the pain start? How long have you had it?
■ Location: Where is the pain? Internal or external? Does it radiate?
Where does it start and where does it radiate to? Is it always in the
same place?
■ Duration: How long does the pain last? Does it come back? How often?
■ Severity: How bad is the pain? (Use an appropriate rating scale.)
■ Pattern: Does anything relieve the pain? What? Does anything make it
worse? Does anything specific seem to cause the pain?
■ Associated Factors or Related Occurrences: Are other symptoms
associated with the pain (headache, visual difficulties, sensitivity to
light, nausea)?
 Causes of Pain
■ Mechanical stress of trauma, surgical incision, or
tumor growth
■ Excesses in pressure, heat and cold
■ Chemical substances released when tissues are
damaged or destroyed
■ Lack of oxygen to tissues
■ Muscle spasms
Factors Affecting Pain Perception
■Pain threshold
– Lowest intensity of a stimulus that causes the subject to
recognize pain
■Pain tolerance
– The point at which a person can no longer endure pain
■Endorphins
– Naturally occurring substances produced by the central
nervous system to relieve pain
 The International Association for the Study of Pain
(IASP): Types of Pain

■ Acute pain or nociceptive pain

■ Referred pain
■ Cancer pain
■ Chronic pain or neuropathic pain
– Limited, intermittent, or persistent
■ Neuropathic
■ Intractable pain
The Pain
Cycle
 TOOTH ACHE

■Dentin hypersensitivity; the pain

arising from exposed dentin,
typically in response to chemical,
thermal, tactile or osmotic stimuli
 TOOTH ACHE

• Unmyelinated C-fibers lied in the pulp

proper
• Myelinated A-fibers lied in the pulp dentin
border penetrated to dentin
• Inflammation may increase the sensitivity
■ Intradental space innervated by A-β and some A-δ
myelinated fibres
– The fluid movement can be quantified by measuring the
hydraulic  conductance of dentin with a high
conductance has a low resistance, and vice versa 
PAIN
■ Sensory innervation only occurs in DENTINAL
TUBULES
– Nociceptors: neuregulin and its ErbB receptors play in
the control of cell morphology and in hyperalgesia
– Evidence demonstrates odontoblasts express mechano-
and/or thermoreceptor (TRPV1, TRPV2, TRPV3, TRPV4,
TRPM3, KCa and TREK-1)  Heat, Cold, or movement of
dentinal fluid
■ Injury  activate and/ or Substance P
sensitise nociceptors 
neuropeptide release in the
periphery  increasing Ca2+
influx  induced
depolarization increase SP
release from sensory
endings
■ Prostaglandins (in inflamed
tissue) bind to their
receptor on sensory fibers
and lower the firing
thresholds of neurons
throughout cAMP and
protein kinase A  enhance
SP release in response to
capsaicin, bradikinin, and
other stimuli
 EFFECT OF SP ON DENTAL PULP
■ SP can be considered as
major mediator of
neurogenic inflammation
and associated hyperalgesia
■ Raising SP in dental
pathologic events:
– Caries
– Pulpitis
– Granuloma
 Vasodilatatory response
 Histamine release
 Increase in blood flow
 Increase in vascular permeability
 Increase in blood pressure
 Synthesis of proinflammatory
cytokines (IL-1, IL-6, TNF)
 Chemotaxis of inflammatory
cells
 Sensitisation of nociceptors
HYPERALGESIA
TOOTH ACHE
Neural Hydrodynamic
Theory Theory
Than
k You