Sei sulla pagina 1di 24

Introduction to Oral Physiology

Physiology of Pain Oral Physiology Dent 207

Physiology & oral physiology




A branch of biology that deals with the study of functions of living matter Oral physiology is the study of the functions of the mouth and associated structures

Functions of the human mouth




The portal to GIT


 

Guiding food intake Preparing food for swallowing and digestion Human trait Requires complicated control of many oral, pharyngeal and laryngeal structures More evident in animals

Speech production
 

Prehensile (holding objects)




Functions of oral cavity are organized


Food analyzed by sensory systems involved in perception of
    

Taste Smell Touch Temperature Pain

 

Sensory information is integrated in the brain, as a result Saliva is secreted


 

Lubrication Calcification - calculus Mastication - occlusion Neuromuscular control of muscle movements Protection from tissue damage

Chewing movements begin


  

Swallowing eventually occurs

Why study oral physiology




 

Knowledge of normal functions of the mouth leads to Explanation of orofacial dysfunction, therefore Suggesting better methods for diagnosis & treatment Practical example of how knowledge of oral physiology has an impact on industry & marketing


Fooling taste system by diet sweets

Pain


Dentistry owes its very beginning to the quest for pain relief Classical foundations of dental profession
  

Identification Diagnosis Elimination of pain

Pain
        

A subjective symptom A reaction elicited by a stimulus May involve a tissue damage Provides a warning to seek treatment Acute vs chronic Spontaneous vs. provoked Continuous vs. intermittent Recurrent periodic Localized spreading migrating - referred

Pain


Definition
 

A complex series of phenomena Unpleasant emotional & sensory experiences associated with actual or potential tissue damage Abnormal affective state aroused by the pathological activity of a specific sensory system

Pain
  

Pain is not simply an excessive stimulation of some other sense such as touch or temperature But instead is related to tissue damage at a cellular level This is why physiologists replace pain with noxious & pain receptors with nociceptors Pain stimulants products of tissue damage
     

Hydrogen ions Potassium ions Prostaglandins Polypeptides Histamine Serotonin

Aspirin blocks the chemical receptors

Nociceptors
  

 

 

Touch & temperature receptors are well defined Pain receptors (nociceptors) respond to painful stimuli Nociceptor is a term used to describe a nerve ending that responds to stimuli that actually or potentially produce tissue damage Nociceptors may respond to very gross mechanical stimuli Other stimuli may result in painful sensation when level of stimulus is increased A single noxious heat stimulus is sensed as painful Repetitive stimulation of temperature receptors with less powerful stimuli may inhibit the passage of pain

A or C fibers


Information originating in nociceptors travels over small diameter afferent nerves (A or C fibers group) Double nature of pain


A faster producing stinging pain (sharp of high intensity initial pain) C slower - producing agonizing intolerable diffuse second pain

A fibers
   

 

Myelinated (2.5 m) Conducting at 12-30 m/s 12High threshold Transmit information from nociceptors or mechanoreceptors Activated by intense mechanical stimulation Involved with 1st pain


Sharp localized sensation from obvious mechanical damage

C fibers
  

NonNon-myelinated (0.4-1.2 m) (0.4Conducting at 0.5-2 m/s 0.5Polymodal




Transmit a number of different stimuli though they are thought to be purely nociceptive in human Excited by intense mechanical, thermal & mechanical Diffuse & dull that follows 1st pain May arise independently

Involved with 2nd pain


 

Pain neuron


Neuron
 

Cell body and dendritic processes Axon Primary Secondary Tertiary

Neurons conducting pain


  

Pain neuron


Primary neuron


Cell bodies in
 

Posterior root ganglia of spinal cord Ganglia of cranial nerves

In the cranial area; all primary neurons conduct pain from pain receptor nerve endings to the Spinal Nucleus of Trigeminal nerve irrespective of the cranial nerve of origin From SN-CN5 to thalamus SNThalamus to cerebral cortex

Secondary neuron


Tertiary neuron


Gate control theory




Stimulation of other sensory receptors at the same time as the nociceptors can prevent the perception of pain gate control theory If the impulses in the nociceptive nerves could proceed up to the cortex, pain would be perceived the pain gate would be opened Explains why pressing on a painful area or clenching on a painful tooth relieves the pain Can explain acupuncture treatment

Indigenous Morphine-like Morphinesubstances


 

Self reading Oral Bioscience, chapter 11: Oral sensation




Page 232 -233

Factors affecting pain threshold




Lowering threshold
 

Psychological factors Fear & worry Excitement & relaxation Soothing music

Elevating threshold
 

Nerve Physiology


     

The conduction of a nerve impulse Nerve cell axon Intracellular Fluid Extracellular Fluid Na and K ions Na and K channels Difference in polarity of interior and exterior of axon

Nerve Physiology


Resting Membrane Potential




A result of the relative distribution of Na and K ions across the axon membrane Intracellularly


[K+] is high, [Na+] is low [Na+] is high, [K+] is low The interior of the axon is -ve relative to the exterior Potential difference of about 60 - 90 mV The natural tendency of Na influx is prevented by Na pump, a process that needs energy

Extracellularly


At the state of rest


  

Depolarisation


Action Potential and Depolarisation


 

Rapid fall in membrane potential from 70 to +20+20-30 mV Nerve impulse (action potential) propagates along the axon and when it reaches the resting segment of the axon it creates an electrical stimulus which increases the permeability of the diffusion barrier to Na and K ions by opening voltage gated ion channels

Depolarization


 

Na+ ions move into cell while K+ ions move out along concentration gradient Intracellular charge is +ve relative to extracellular This segment of the axon has undergone depolarisation and is in a state of action potential As depolarisation progresses along the axon the action potential is propagated and the nerve stimulus continues down the length of the axon

Repolarisation


 

The axon returns to its original state with initial concentrations of Na and K ions restored and the interior once again -ve relative to the exterior This is achieved by the Na and K channels The axon is ready to undergo depolarisation again to propagate a nerve impulse Active process that takes up energy

Mechanism of action of local anesthesia




Blocking of the Na ion pumps in the cell membrane wall This results in an inability for Na ions influx when the action potential arrives at a given segment of the nerve No effect on resting potential