oral physio script 3

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    Oral physiology 2012lecture note 3

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    We continue last weeks slides.

    Substance P is important for conduction of pain or nocicetive response.They are important for

    triggering pain,or for initiating the response of pain.Pulp reacts initially to stimulating dentine.Itreacts ;

    Electrically - example ; when we examining the pulp electrically.(by using a device in clinic) Mechanically - example ; when we make a caries (by drilling) within the tooth. Chemically - example ; when we have caries in dentine.

    Although we only stimulate dentine,but the pulp also will response because pulp and dentine is

    within a one system.

    When we stimulate dentine,C fibres are stimulated.This retrograde impulse in C

    branches.(retrograde means opposite to the usual order,inverted or reversed.)And this,lead to

    vibration or release of substance P at the terminals of the fibre.Substance P is a vasodilator.It will

    cause vasodilation which leads to tissue edema.(edema : accumulation of fluid inside the

    tissue).Also,release of substance P lead to release of histamine.(Histamine is an important substance

    that lead to vasodilation and lead to increase the permeability of capillary and cause fluid

    extravasation).

    Bradykinin is another substance that important for initiation of pain.It is important for the noxiousstimulation of the pulp.When bradykinin is release,it also cause vasodilatation and it may stimulate

    release of encephalins from pulpal cells.

    Encephalins are anti-inflammatory.Because it is an anti-inflammatory,it will inhibit bradykinin

    release.This is how dental pulp decrease its inflammation.It is a kind of protection as it undergoes

    negative feedback mechanism.

    We also have ecosanoid group,these are metabolite of arachidonic acids.We have prostaglandins

    and leucotrienes.These are also important for initiation of pain to dental pulp.

    Prostaglandins I2 is produced by endothelial cells (cells that are lined the blood vessels).It inhibit

    platelet aggregation and also a vasodilator.Thats why prostaglandind are important metabolites to

    increase inflammation.

    Also we have thromboxane A2.It is produced by platelets and fibroblast.This stimulate platelet

    aggregations.In the pulp we have PG I2, PG F2 , PG E2,in addition to Thromboxane A2 and

    Leucotrience 12-HETE, LTC4 . All of these will cause nociceptive response in the pulp.

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    And bacterial or mechanical or chemical irritation in the pulp will increase in prostaglandins

    release.This also will lead to vasodilatation and lead to increase in pain-producing properties of

    histamine,bradykinin and serotonin.

    Now,why we take pain relieving drugs?We take aspirin or painkillers but hw does this drugs

    function?Aspirin for example is an inhibitor of cyclo-oxygenase enzyme which lead to inhibition of

    prostaglandins synthesis.Thats why when you take aspirin,you reduce the amount of prostaglandin

    synthesis and thats why you reduce the amount of inflammation.Remember prostaglandins is a

    vasodilator,also it leads to release of histamine,bradykinin and serotonin.Thats why aspirin is one of

    the important drugs,but aspirin is know not use very much as a painkiller because it is also an

    important property of blood.It inhibits platelet aggregation so thats why it is an anti-coagulant.

    Root canal medicaments is use during root canal treatment (RCT).Usually we give the medicaments

    in between the visits.This medicaments inhibit synthesis of PG and leucotrienes and have

    antibacterial activity as well.Eugenol is more effective than phenol in inhibition of prostaglandin

    synthesis.It reduces the amount of pain.

    Increase in prostaglandin synthesis = increase in pain

    Injury to dentine due to cavity preparation,

    what will happened?

    Nerve fibres and odontoblastic processes are pulled out by hydrodynamic force, this will lead to

    separation of them from pulpal tissue. Damaging nerve fibres and killing of odontoblast will leave

    pain in dentine. This is why if you want to drill in dentine, you cannot do that without giving

    anaesthesia to the patient. It will be very painful.

    In small injury, such as tear for example , dentine itself start to build layers which block the dental

    pulp from the sources of injury , this is called reparative dentine which is dentine that have been

    built to repair loss of dentine. If the area is huge and its fast , it can lead to inflammation of dental

    pulp and pulp necrosis. The reparative dentine may seal off any small damaged areas, which blocks

    re-innervation and cause innervations of adjacent areas to increase.

    Doctor said dont worry about the last two sentences in slide 20. They are not important.

    The pulpitis is when the cavity reach the pulp, or you are drilling into the dentine then suddenly you

    are in the dental pulp.

    What will happened?

    Odontoblastic layer will destroyed which allow inflammation to occur locally.

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    In small lesions, dentine bridge forms which preserve the pulp and heal it , this is called reversible

    pulpitis. The pulp will heal and return back to normal condition.

    If the opening to the pulp is really huge, and the number of stimuli affected is severe, this is what we

    called irreversible pulpitis. This pulpitis will not go back to its normal state.

    And finally after the pulpitis, we should go to pulp necrosis. ( slide no 22)

    Irreversible pulpitis will not gain its normal state, so it will stay in that state for a while until the

    necrosis occurs. This pathogen will spread to dental pulp to surrounding periodontal ligament and

    they will produce further inflammation. Inflammation area are demarcated by fibrous tissue. This

    will lead eventually to pulp necrosis. This mean more pulp necrosis occur in more severe pulpal

    exposure. This appear after the irreversible pulpitis. Thats why in dentistry, if you diagnosed pulp

    having irreversible pulpitis, the treatment is root canal treatment ,before that you can treat the

    tooth by filling.

    What happened if the pulp necrosis?

    It can remain for a while but in future, this pathogen exist in the pulp can break out and induce what

    we called periendo inflammation. So the lesion extend to root apex, nerve growth in periapical area,

    and new fibers appear to be involved in pain stimulation. This mean more pain fiber growth in the

    area surrounding the periapical tissue and this will be responsible for more pain in the area.

    Pain of Dental Origin (slide #23)

    1) Exposed dentine sensitivity - painExposed dentine is sensitive. Sometimes the tooth may fracture off. Dentine is exposed, so

    because of that, you feel pain. Exposed dentine is one of the major problems in dentistry.

    Sometimes dentine is exposed because in the root, the surface layer of cementum that covers

    the root is worn out, and this occurs in all age. This cemental layer covering the root is very

    thin, so it can be lost easily, by tooth brushing for example. Or you can expose the dentine by

    cavity preparation, dental caries or fracture of the crown.

    2) Any sensation through dentine may cause pain**Do remember that the point were talking about is very important and there will be questions

    about that in the exam.

    3) Heat / cold may be perceived as separate sensations?Do you feel heat or temperature in the dental pulp? Ya3ni do you have receptors for thermal or

    mechanical stimuli in the dental pulp? The answer is NO~! The only response in the dental pulp

    is PAIN. In the dental pulp, we only have pain receptors. Thats why if you eat an ice cream, you

    may feel that you feel temperature but it is not. It is actually pain. (The doctor keeps on

    emphasizing that we ONLY have pain receptors in the dental pulp, NOT thermal or mechanical

    stimuli.)

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    But one student may raise his hand up and says when I eat an ice cream in the summer, I feel its

    temperature or coldness. Actually this is because it affects the mucosa or the area surrounding

    the tooth, NOT because of the effect of temperature on the tooth itself.

    4) Most sensitive areas in dentine as ata. enamel-dentine junction (EDJ)b. Exposed dentine in cervical root areas

    5) Nerve fibers to dentine are limited to coronal dentine6) Nerve fibers numerous under cusps

    And that is why the area of dentine just under the cusps is very sensitive.

    7) Nerve fibers extend for a short distance within dentine8) Odontoblastic processes vary in extension through dentine

    In addition to the nerve fibers that extend through the teeth, we have processes that are called

    the odontoblastic processes.

    Just remember, if youre asked in the exam, what are the structures that may extend through the

    dentine? Only TWO things: thenerve fibers and the odontoblastic processes.

    Three theories of dentinal hypersensitivity (Slide #24)

    We have three theories;

    1) Odontoblastic processes as receptorsWhy? Because the odontoblasts arise from the neural crest themselves. These neural crest cells

    are neural, so thats why the odontoblastic cells may function as nerves, in conduction or in

    receiving pain.

    2) Nerve fibers extend through dentinea. Direct stimulationb. Deformation of odontoblasts by fluid movement promotes potassium release action

    potential in neighboring nerve fibers

    3) Hydrodynamic theoryThis is the most acceptable theory. We have fluids inside the teeth. Because of the movement

    of the fluids, this actually leads to stimulation of the nerve fibers at the area of the Raschkows

    plexus.

    Remember that the third theory (hydrodynamic theory) is the most acceptable theory of dentinal

    hypersensitivity, which says that we have movement of fluids in and out, within the dentinal tubules.

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    Referred pain (Slide #25)

    Referred pain - when you feel the pain not exactly in the area where tissue damagehappens. For example, we should have pain in the tooth, but instead of feeling the pain

    inside the tooth, you feel the pain in your head. So you have headache instead of tooth

    pain. Please remember that referred pain is different from migrating pain.

    Migrating pain You start to feel the pain in the tooth and this pain migrates to another area. Spreading pain - the pain starts in the tooth and spreads to another area but it is still in the

    tooth.

    There will be questions about these terms in the exam and you should be able to distinguish

    between them.

    Okay. Why does referred pain take place? Sensation of pain resulting from a deep organ peripherally

    in areas derived from the same somite. Sometimes, we hear that people who have pain in the chest

    spreading to the left arm, suffer from heart attack. Why does this pain appear at the arm? What

    does the arm have to do with the pain? This is an example of a referred pain.

    REFERRED PAIN

    Before heart attack, the patients suffered from angina pectoris. The pain appears in the left

    arm instead of appearing in the heart. This is referred pain. It appears there because the

    area or the source of pain and the site where the pain appears (referred pain) originate

    from the same somite. In Histology, we said that somite is from paraxial *****. If two

    tissues originate from the same somite, we can see referred pain in one of these tissues.

    When the pain starts, it should be in the first tissue.

    The convergence of somite and the visceral sensory impulses may take place at one or more

    of three levels. For example, a pain appears in the head instead of appearing in the tooth

    because the area on the skin of the head is from the same somite as the area of the tooth.

    Because of that, this pain will travel to the brain. They will converge at some distant and

    they will have a common path.

    This convergence can be :-

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    1) prespinal (before spinal cord)

    2) spinal (at the spinal cord)

    3) supraspinal (above the spinal cord)

    Here we talk about referred pain from the body, but not from the head.

    REFERRED OROFACIAL PAIN

    When we talk about referred pain from the head (from the head region or from the face,

    upper and lower jaw), this convergence can be :-

    1) prepontine ( before the pons)2) pontomedullary (at the area of the pons and medulla oblongata)3) suprapontine (above the pons)

    There are nerve fibers from the stem and from the skin of the head that meet. This meeting

    can be at the pons, before the midbrain, within the midbrain, or above the midbrain. There

    is no convergence within the brain. Once the nerve fibers reach the thalamus, the will pass

    from the thalamus to the peripheral cortex.

    Pain within the oral cavity is referred within the distribution of the specific divisions of the

    trigeminal nerve. This means that the pain within the oral cavity can appear anywhere

    within the specific divisions of the trigeminal nerve. That is why we can feel the pain in the

    skin for example. The pain can also appear as headache. Referred pain cannot across the

    midline, except in ramifications of nerve terminals (incisor region). If we have headaches

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    on the right sides of our heads, do not look for any tooth on the other side. The tooth that if

    responsible for this pain should be at the same side. However, headache in right side maybe

    referred to the left side of incisor, but not molar.

    Migrainous headache maybe due to dental conditions but it is not a referred pain because it

    is vascular in origin.