Cranio Notes

L1: Introduction to lab workflow for splints

- Preparation of casts
o Mark the maximum perimeter and the gingival margin. Mark the palatal
margins
o Liquid wax covers the undercuts, interdental spaces and curves that prevent
the detachment of the acrylic from the gypsum. It is possible to have a splint
made using digitally printed casts with small differences in the management
of the acrylic in order to enable the detachment of the heat cured acrylic
from the acrylic of the cast
o The bite registration process in the clinic was done in the position that the
patient is intended to use the splint, ie for a bruxer with increased activity at
sleep, the bite registration is in the closing trajectory of the mouth and the
patient is placed at supine position (horizontal position) with aluminum wax
block
o Casts are mounted according to the bite registration (that also defines the
thickness of the splint)
§ The maximal perimeter is defined on the dental arch that the splint
will be placed
§ We also draw a line along the gum line as guidance for the mounting
- Boxing: we follow the lines we draw prior to stick the wax
- Soak casts post boxing, in a bowl with room temperature water for 10 mins
- Base and catalyst to fabricate the splint
o Base of heat cured acrylic-> This is a heat cured acrylic that is added
gradually piece by piece, at the different sections of the dental arch
o Catalyst
- The splint is soaked as it is (on the cast and the articulator), in a bath of water
(temperature 40oC) for 20 mins
o Pressure polymerization unit
o This step is important to keep the dimensions of the splint steady
- Begin regulating the contacts. Firstly mark all the incisal edges and casp tips with a
pencil
- Finishing and polishing
o The polishing paste contains volcanic dust and is soluble in water
§ Finished and polished splint
§ The it is sprayed with alcohol for disinfection and it is ready
- Athletic splint
o The bite registration is taken at a vertical position on the dental chair, since
this is the position that the pt will be using the splint
o Confirm that your pt can swallow using this particular thickness
o The 1st silicone sheet is heated in a certain temp as instructed by each
company-> The heated sheet is guided on top of the cast
o The 1st layer is cut and shaped. The material is perforated to avoid the air
trapping at the adjustment of the 2nd layer of silicone
 o The 2nd layer is heated at the vacuum machine and adjusted on top of the 1st
layer. The warm material is glued through the heat on the lower one, and its
margins are hugging gently the lower layer

L 2: Basic Knowledge from physiology of the SS

- The SS is composed of
o The dentition
o The skeletal str (mandible, maxilla,
condyle, glenoid fossa etc)
o The two TMjs
o The M and the ligaments
o Remember: masticatory system = SS
(equal terminology)
- TMJ = Temporomandibular joint
o It is the point were temporal bone and the mandible are articulated and form
a joint
o TMJ is unique joint because
o It is a ginglymoarthrodial joint (hinging and gliding movements) – movement
in 3 planes -> movement: rotation- downwards – frontal and inwards. Other
joints of the body normally move in 2 planes max
o The two TMJs normally function as a pair, at the same time
o The articular eminence, the temporal fossa and the condyle are covered with
collagen fibres (other joints: hyaline covers the articulated surfaces)
o The articular disc serves as a non- ossified bone that permits complex
movements of the mandible
o In the textbooks the TMJ is also referred as a synovial joint
o Synovial joint = Diarthrosis (equal terms)
o A synovial joint is the type of joint found between bones that move against
each other, such as the joints of the limbs (shoulder, hip, elbow and knee).
Characteristically it has a joint cavity filled
with fluid
o 3 main features of a synovial joint are
§ Articular capsule: surrounds the joint
and is continuous with the
periosteum of articulating bones
§ Articular cartilage
§ Synovial fluid
o Non synovial joints
§ Fibrous/ synarthrosis (cranial sutures,
bonds between roots of teeth and jaw
bones)
§ Cartilaginous/ amphuarthrosis (manubriosternalis and pubic)
o Articular disc
§ Serves as a non- ossified bone that permits complex movements of
the mandible
§ It is made of dense fibrous CT
§ Thinner in the middle, thicker at the periphery
 § Posterior to the posterior border bilaminar zone of is innervated and
vascularized
§ Attrition of the articular disc -> arthritis
§ The retrodiscal (bilaminar) zone is located between the post band of
the TMJ disc and the posterior portion of the TMJ capsule. The
‘bilaminar’ refers of the two posterior attachments of the disc
• Superior layer – elastic allow anterior translation of the disc
over the articular eminence
• Inferior layer (collagen) – inelastic to maintain relationship
with condyle
§ What is the role?
• Absorption of pressure
• Protection of the osseous str of TMJ (condyle and temporal
fossa)
§ What is the appropriate exam to locate the position of the articular
disc in the TMJ?
• MRI = most preferable + Ultrasound
§ Why is radiography excluded as a possible exam to locate the disc?
• Radiography (OPG) shows only the osseous str NOT the soft
tissues
o Reminder
§ Unilateral – when just one part of sth, or just one side of sth
participates
§ Bilateral – when both parts or sides of sth participate
§ Contralateral – when a part/ str of one side acts, but the result shows
at the opp side
§ Ipsilateral – when a part/ str of one side acts and the result shows at
the same side
o The vessels and the nerves of TMJ
§ Innervation of TMJ-> Branches of trigeminal V
• Auriculotemporal (branch of mand n)
• Deep temporal
• Deep masseteric
§ Vasculature
• Superficial temporal
• Internal maxillary
• Deep auricular
• Anterior tympanic
• Ascending pharyngeal
o The ligaments
§ Ligaments + M + soft tissues => hold the mand below the cranium
§ Role = protection
§ Do not stretch when SS functions normally. If a parafunction is
prolonged, then the ligaments may stretch and be deformed
§ Main ligaments of SS
• Capsular
 • Temporomandibular
• Sphenomandibular -> Limits the distension of the mandibule
inferiorly
• Stylomandibular-> Limits excessive protrusion
- The M of the MS
o Primary M
§ Masseter
§ Temporalis
§ Lateral pterygoid (with 2 heads)
§ Medial pterygoid
o Secondary M
§ Sternocledomastoid
§ Suprahyoid
§ Inferior hyoid
§ Trapezius
§ Semispinalis capitis
o Remember
§ Lateral pterygoid M: Has 2 heads, superior + inferior
• Superior head – 2 origins
o Anterior part of the articular disc
o The infratemporal surface of the infratemporal surface
of the infratemporal crest of the grater wing of the
sphenoid bone
• Inferior head – 2 origins: Condyle + Lateral pterygoid plate
§ Digastric M
• Origin:
o anterior belly- digastric fossa on mandible
o posterior belly – mastoid notch on the temporal bone
• Insertion: common tendon to hyoid bone
• Action: assists in depressing the mandible (opening the
mouth) + elevates and steadies hyoid bone during swallowing
and speaking
• Innervation
o Anterior belly – mylohyoid n (which is traced back to
CN V)
o Posterior belly – Facial nerve (CN VII)

Action M activated
Elevation of jaw (closing of mouth) Masseter, temporalis, medial pterygoid M
(bilateral action)
Depression of the L jaw (opening of mouth) Lateral pterygoid M, anterior digastric M,
mylohyoid M, geniohyoid M, stylohyoid M,
mimic M (bilateral action)
Protrusion (forward movement of the L BOTH lateral pterygoid m (bilateral action)
jaw)
Lateral movement of the jaw (movement at Opposite lateral pterygoid M (contralateral
one side) activation of the LP M)
- Glossary of prostho
o Centric relation : A maxillomandibular relationship, independent of tooth contact, in
which the condyles articulate in the anterior-superior position against the posterior
slopes of the articular eminences; in this position, the mandible is restricted to a
purely rotary movement; from this unstrained, physiologic, maxillomandibular
relationship, the patient can make vertical, lateral or protrusive movements; it is a
clinically useful, repeatable reference position.
§ Remember
• CR is not about teeth. It is about the position of the condyles
• CR is repeatable and reproductable
§ Methods to determine CR
• Bilateral manipulation
• Anterior bite stops
o Directly fabricated anterior deprogramming device
o Pankey jig
o Lucia jig
o Best- bite appliance
• Leaf gauge
• Nociceptive trigeminal inhibition
• TENS as in physiotherapy to relax M
§ Loading of TMJ – Test CR
• Principle: if the TMJs are not completely comfortable when firmly
loaded, they are not in CR
§ Functional O from TMJ to smile design
• The mand is in CR if 5 criteria are fulfilled
o The disk is properly aligned on both condyles
o The condyle- disk assemblies are at the highest point possible
against the posterior slopes of the eminentiae
o The medial pole of each condyle- disk assembly is braced by
bone
o The inferior lateral pterygoid M have released contraction and
are passive
o The TMJs can accept firm compressive loading with no sign of
tenderness or tension
§ Adaptive CR
• Centric relation is the accepted term for defining the condylar axis
position of intact, completely seated, properly aligned condyle-disk
assemblies. A TMJ that is structurally deformed with a misaligned or
displaced disk cannot be described as in centric relation because it
does not fulfil the critical requirement of a properly aligned disk.
However, some structurally deformed temporomandibular joints
(TMJs) may function comfortably even though they do not fulfil the
requirements for centric relation.
• Like centric relation, adapted centric posture is a horizontal axis
position of the condyles. It occurs irrespective of vertical dimension or
tooth contact.
 • Adapted centric posture is the manageably stable relationship of the
mandible to the maxilla that is achieved when deformed TMJs have
adapted to a degree that they can comfortably accept firm loading
when completely seated at the most superior position against the
eminentiae.
• The mandible is in adapted centric posture is 5 criteria are fulfilled
o The condyles are comfortably seated at the highest point
against the eminentiae
o The medial pole of each condyle is braced by bone (the disk
may be partially interposed)
o The inferior lateral pterygoid M have released contraction and
are passive
o The condyle to fossa relationship is manageably stable
o Load testing produces no sign of tension or tenderness in
either TMJ
§ PS: For not you do not have to know in detail the following – diff lecture in
intracapsular disorders
• Some of the most common intracapsular disorders that can evolce
into an adapted Centric posture include
o Lateral pole derangements
o Complete disk derangement with formation of a pseudo disk
o Complete disk displacement with perforation
o Other partial disk derangements and clicking TMJs
o Maximal intercuspal position (MIP): The complete intercuspation of the opp teeth
independent of condylar position, sometimes refered to as the best fit of the teeth
regardless of the condylar position
o Interocclusal rest distance: The difference between the rest vertical dimension and
the occlusal vertical dimension
§ Syn interocclusal rest space,
§ Comp interocclusal distance
o Freeway space: Syn interocclusal rest distance, interocclusal rest space
§ = RVD– VDO
o Centric occlusion: The occlusion of opposing teeth when the mandible is in centric
relation; this may or may not coincide with the MIP
o Centric position: The position of the mandible when the jaws are in CR
o FC vs NFC
§ In normal conditions the FC are the L cusps of upper back teeth and the B
cusps of the lower back teeth
§ They determine the height of the lower face at the sagittal plane!!! -> the
vertical dimension
§ FC = centric cusps
§ NFC = non centric cusps
o Occluding str in normal O
o Protrusion = a position of the mand ant to the CR
without lateral deviation
§ A protrusive force moves the mand forward
 § Clinically there is no deviation from the middle line of the face
o Lateral
§ Positions either right or left of the midsaggital
plane
§ Denotes a position farther from the median
plane or midline of the body or str
o Lateral movement of the jaw (laterotrusion): A
movement from either R or L of the midsaggital plane
o WS vs NWS
§ WS= side towards there is a movement of the
jaw. | The condyle at the WS is called
functioning condyle
§ NWS = side that is opp of the side of the movement | The condyle at NWS =
non functioning condyle
o 3 planes of motion
§ Frontal/ coronal plane
§ Sagittal
§ Transverse/ horizontal
o What is occlusion?
§ The act or process of closure or of being closed or shut off
§ The static relationship between the incising or masticating surfaces of the
maxillary or mandibular teeth or tooth analogues
§ Is O a term that describes teeth relationships in normal function of the SS?
§ Dynamic O
• Is O a term that describes teeth relationships in normal function of
the SS? No
o O describes the way all parts and str (dentition, M, TMJs) of
the SS are related under any conditions (function,
parafunction, dysfunction, mastication, swallowing)
o Occlusal force = the result of muscular force applied on opposing teeth; the force
created by the dynamic action of the muscles during the physiologic act of
mastication; the result of muscular activity applied to opposing teeth
o Occlusal contact = 1. the touching of opposing teeth on elevation of the mandible; 2.
any contact relationof opposing teeth
o Occlusal analysis = a systematic examination of the occlusion with special
consideration to the interocclusal Relations of mounted casts
o Occlusal balance = a condition in which there are simultaneous contacts of opposing
teeth or tooth analogues on both sides of the opposing dental arches during
eccentric movements within the functional range
o Occlusal disharmony = a phenomenon in which contacts of opposing occlusal
surfaces are not in harmony with other tooth contacts and/or the anatomic and
physiologic components of the craniomandibular complex
o Occlusal dysesthesia = unusual sensory Perceptions during occlusal contact
o Occlusal equilibration = the modification of the occlusal form of the teeth with the
intent of equalizing occlusal stress, producing simultaneous occlusal contacts or
harmonizing cuspal relations
 o Function = any normal activity performed without complications on SS (mastication,
deglutition, speech)
o Parafunction = oral parafunction includes bruxism, clenching, lip biting, thumb
sucking and any other oral habit not associated with mastication, deglutition and
speech
o Dysfunction = the presence of functional disharmony between the morphologic form
(teeth, occlusion, bones, joints) and function (muscles, nerves) that may result in
pathologic changes in the tissues or produce a functional disturbance

W 3: Aetiology of TMDs
- Types of occlusion
o Angle’s types of malocclusion (Class I, II, III)
o Group function occlusion
o Cuspid (canine) guided occlusion
- Common occlusal relationships of posterior teeth
o Class I
§ The following char identify the most typical molar relationship found
in the natural dentition, first described by angle as a Class I
relationship
• The MB cusp of mand 1st M occludes in embrasure area
between max 2nd PM and 1st M
• The MB cusp of max 1st M is aligned directly over the B groove
of the mandibular 1st M
• The ML cusp of max 1st M is situated in the CF area of mand 1st
M
§ In this relationship each mand tooth occludes with its counterpart and
the adjacent M tooth
o Class II
§ The MB cusp of the mand 1st M occludes in the CF area of max 1st M
§ The MB cusp of mand 1st M is aligned with the B groove of max 1st M
§ The DL cusp of max 1st M occludes in the CF area of mand 1st M
§ When compared with Class I relationship, each O contact pair is
situated D, approx. the MD width of a PM
o Class III – result of a predominant growth of mandible
§ The DB cusp of mandibular 1st M is situated in the embrasure
between the max 2nd PM and 1st M
§ The MB cusp of the max 1st M is situated over the embrasure between
the mand 1st and 2nd M
§ The ML cusp of max 1st M is situated in the M pit of the mand 2nd M
o Angle’s classification
§ Normal: MB cusp of upper 1st M occludes with B groove of lower 1st M
§ Class I: same as normal but char by crowding, rotations and other
positional
 § Class II: the MB cusp of upper 1st M occludes anterior to the B groove
of the lower 1st M. There are 2 subtypes of Class II
• Class II div 1 – upper incisors are tilted outwards, creating
significant overjet
• Class II div 2 – upper incisors are labially inclined
§ Class III: the MB cusp of the upper 1st M occludes posterior to the B
groove of the lower 1st M
Class II div 1 Class II div 2
Upper incisors are proclined Upper central incisors show lingual inclination and
may be overlapped by upper lateral incisors
Excessive overjet and deep overbite Deep overbite
V- shaped upper arch, narrow in Broad upper arch (usually)
canine region
Broad between M
Shorter upper lip – failure in anterior Normal upper lip and lip seal Deep mental groove
lip closure
Mandible may be deficient and chin Mandible is of a good size
underdeveloped

o Pseudo class III

§ Dental, the upper incisors are retroclined with normal or protruded
lower incisors
§ It is an anterior cross- bite
§ Posterior teeth usually have Class I Occlusal relationship
• Pts thruss their tongue
• Not a skeletal problem but a habit that caused that problem
o Group Function
§ Multiple contact relations between maxillary and mand teeth in
lateral movements on the WS whereby simultaneous contact of
several teeth acts as a group to distribute O forces
§ Explaining the terminology
• The are contacts between the anterior (not always) and
posterior teeth of the two dental arches at the working side,
and there are no contacts at the non-working side.
• At least 2 pairs of posterior teeth guide the movement at the
working side
• The forces during lateral movement of the jaw are distributed
only at the working side.
§ Explaining the group function
• The are contacts between the anterior (not always) and
posterior teeth of the two dental arches at the working side,
and there are no contacts at the non-working side.
• At least 2 pairs of posterior teeth guide the movement at the
working side
• The forces during lateral movement of the jaw are distributed
only at the working side.
 o Canine guidance: Syn Canine protected articulation
§ A form of mutually protected articulation in which the vertical and
horizontal overlap of the canine teeth disclude the posterior teeth in
the excursive movements of the mandible
§ Syn anterior protected articulation
§ Explaining the canine protected articulation
• The canines –each one separately- disocclude the posterior
teeth at lateral excursions of the mandible, ie during a lateral
excursion there is only one contact between the canines of the
working side.
• disocclude = disengage = they are not in contact
- Occlusal interferences = 3 types
o Occlusal interference of a certain Occlusal scheme (group function/ canine
guided): It is an undesirable contact at the NWS (balancing) during lateral
excursion of the mandible
o Premature O interference: It is a deflective O contact that appears on recent
high restorations
o Deflective O contact: Centric interference usually due to natural causes
(tooth acial direction, tooth eruption)
§ A contact that displaces a tooth, diverts the mandible from its
intended movement or displaces a removable denture from its basal
seat
- FC vs NFC
o Role of FC: Together with NFC, they are responsible for mastication and
shearing of food
§ They maintain the distance between the mandible and the maxilla
(vertical facial height- vertical dimension of occlusion)
o Remember
§ The area of a centric cusp is around 1mm2
§ The outer aspect of the centric cusp has a functional significance,
why?
o Role of NFC
§ They assist the centric cusps in shearing food during mastication
§ They keep the bolus on the O table during mastication
§ They minimize tissue impingement
§ They provide mandibular stability
o In an adequate O the B cusps of the lower back teeth Occlude
§ On the L cusps of upper back teeth
§ On the central fossa of upper back teeth
o Synonyms
§ FC = supporting cusps = centric cusps
§ NFC = Non supporting cusps = non centric cusps (eccentric cusps)
- Ideal O vs Normal O
o Characteristics of the ideal occlusion
§ All the teeth of the mandible apart from the central incisor and the 3rd
M, occlude with 2 teeth of the upper dental arch in Max ICP
 § The O stability occurs bec there are equally distributed forces in both
dental arches
§ The vertical dim (sagittal distance) is preserved by the B cusps of the
lower dentition and the L cusps of the upper dentition
§ The B cusps of the upper post teeth and the Lingual cusps of the lower
posterior teeth do not occlude with the opp teeth, they just take part
in normal functions of the SS (mastication)
§ The incisal edges of lower incisors occlude slightly with the Lingual
surfaces of the upper incisors
o Char of Normal O (also called Adequate O)
§ It is any type of O that differs obviously from the perfect O but there
is NO manifestation of dysfunction of SS
§ The teeth are placed in the dental arches in a way that the loads of
forces are equally distributed, and the forces are directed to the
vertical axis of the teeth
§ The lateral motions are performed without any O interferences
§ In resting position there is enough space between the upper and
lower arch
§ The placement and morphology of the teeth are not a reason of
complaints
o Mutually protected articulation: an O scheme in which the posterior teeth
prevent excessive contact of the anterior teeth in MIP and the ant teeth
disengage the post teeth in all mand excursive movements
§ Key phrase – the posteriors protect the anterior, the anteriors protect
the posterior
§ Syn mutually protected O
- The role of O in TMDs
o Based on the knowledge you obtained the previous y as students of dentistry,
do you think that O causes TMDs? HOMEWORK
o At this point go to the articles!!!
§ Occlusion on its own cannot cause TMDs but it is multifactorial
§ Bad O can exaggerate a problem there is always a background
o Post theories
§ Traumatic O contact theory: The traumatic O contact theory suggests
that O discrepancies (premature or excessive contact between teeth)
contribute to the development of TMDs by placing excessive or
uneven forces on the TMJ and associated M
§ Avoidance of tooth contact theory
o O adjustment approaches used in past
§ Freedom in centric (or long centric)
§ Excursive guidance scheme
§ O contact scheme: Emphasized on
tripodization
• An O scheme characterized by a
cusp to fossa relationship in which
there are 3 points of contact
about the cusp and opp fossa with no contact on the cusp tip
o How does the envelope of motion changes?
o Tripodization: an O scheme char by a cusp to fossa relationship in which
there are 3 points of contact about the cusp and opp fossa with no contact
on the cusp tip
o Mand movements on the
sagittal plane (vertical)
§ The envelope of motions
by posselt
o How does the envelope of
motion changes?
§ Freedom in centric or
long centric: it is a
relatively flat area
created between the CR
and the CO positions, on the O surfaces of the teeth (from hinge
position to habitual intercuspal position)
o There was a false belief in 1960s that O on its own could cause a TMD, that
derived from questionable clinical trials
o What we know today: there is no proof that O is the principal factor that
causes TMDs. On the contrary, there are individuals who have Occlusions
that are nowhere near perfect O and they never developed a TMD
o The current theory on the aetiology of TMDs = MULTIFACTORIAL
§ Anatomic (type of O, iatrogenic occlusion, bone morphology – shape
of condyle, shape of mandible, angle of mand)
§ Neuromuscular (the M and n of the SS are involved in mech of apin
and reflexes, that due to increased loads of the TMJ and the
masticatory system, can lead to chronic muscular fatigue or central
sensitization)
§ Psychological (stress, anxiety, depression, personality traits => lead to
parafunctions that result in dysfunction of SS)
§ When at least 2 of the 3 factors have a more dominant role -> TMD
• N + A = TMD
• N + P = TMD
• A + P = TMD
§ Another classification – the factors inv in
TMDs
• Initiating factors
o Trauma (TMJ injury, O
trauma – iatrogenic)
o Parafunctions (recent)
• Predisposing factors
o Occlusion
o Psychological factors (stress & personality traits)
o Macrotrauma
o Hormonal factors
o Parafunctions (chronic)
o Joint hyperlaxity and hypermobility
 o Hereditary factors
• Perpetuating factors
o Behavioral factors: grinding, clenching, head posture
o Social factors: response to pain
o Emotional factors: depression, anxiety
o Cognitive factors: individual issues and anything that
has to do with the way someone perceives and
portrays himself
§ The following O factors showed a possible correlation with TMDs
• Posterior cross bite
• Overjet/ overbite >5mm
• CR/ MI sliding >2mm
• Edge-to-edge bite
• Anterior cross bite
• 5 or more missing teeth

W 4 – Lab Delivery of Slpint

- Tools you need
o Straight hand piece
o Articulating paper
o Burs for acrylic
o Air syringe
- Burs you need
- What happened until delivery
o Preparation of casts
§ Mark the max perimenter and the gingival margins. Mark the palatal
margins
§ Liquid wax covers the undercuts, interdental spaces and curves that
prevent the detachment of the acrylic from the gypsum
§ Casts are mounted acc to the bite registration (that also defines the
thickness of the splint)
• The max perimeter is defined on the dental arch that the splint
will be placed
• We also draw a line along the gum line as guidance for
mounting
o Boxing – we follow the lines we draw prior to stick the wax
o Soak casts post boxing, in a bowl with room temperature water for 10mins
o Base and catalyst to fabricate the splint
§ Base of heat cured acrylic + Catalyst
o The splint is soaked as it is (on the cast and the articulator), in a bath of water
(temp 40oC) for 20mins
§ Pressure polymerization unit
§ This step is important to keep the dimensions of the splint steady
o Begin regulating the contacts. Firstly mark all the incisal edges and casp tips
with a pencil
o Finishing and polishing
§ The polishing paste contains volcanic dust and is soluble in water
 § Finished and polished splint
§ Then it is sprayed with alcohol for disinfection and it is ready
st
- At the 1 appt
o Pt in horizontal position – as per bite registration and how the pt will use it
o ALWAYS CHECK THE SPLINT IN THE PTS MOUTH
o ALWAYS ADJUST THE CONTACTS
o Before you do anything -> mattify the surface
o Burs aggressive one mattify the whole surface because the articulating paper
will not show anything on the acrylic splint
- Step 1
o Check the adjustment and placement on the dentition
o Relax the parts that give discomfort to the pt (always begin from the anterior
teeth- close to the max perimeter and at the labial surface of the anteriors-
try to avoid as much as possible the posterior teeth)
o At the first appt we only adjust the contacts as max intercuspation on the
splint
- Step 2:
o Take the articulating paper and check the contacts. Prefer the U shape with
the 2 different colors at each side
- Step 3 (need to balance it and get the same amount of contact points in both sides)
o Try to give contacts nearly everywhere on the occlusal surface
o Begin by eliminating the highest points on the occlusal surface, because this
will gradually increase the number of contacts from the antagonists
o After every elimination you use the articulating paper to check the contacts
- Step 4
o Try to give contacts nearly everywhere on the occlusal surface
o Try to give contacts that correspond to the supporting cusps and eliminate
the contacts that correspond to the non- supporting cusps
o Which dot would you eliminate? For upper arch
§ Check in mouth – which are pts supporting cuspls
§ Need to eliminate the B – we want the P
o At this point you check in the mouth which are your pts supp (centric) cusps
of the antagonist (on the lower arch), and you keep in mind! The supporting
cusps based on your pts occlusal scheme are the contacts that you want to
see on the occlusal surface
§ Final step of the first appt
§ It is not necessary to have contacts everywhere, as long as the
contacts are balanced and they do not disturb the occlusal surface of
the splint to the point that this changes the occlusal scheme
§ If you have a patient with adequate occlusion, where the supporting
cusps of the lower arch are as expected the buccal cusps -> double
check it in the mouth -> confirm that the contacts that you see on the
occlusal surface of your splint correspond to your supporting cusps
- It is not necessary to have contacts everywhere, as long as the contacts are balanced
and they do not disturb the occlusal surface of the splint to the point that this
changes the occlusal scheme
L4: Masticatory M disorders – Myogenous pain
- Myogenous pain = any pain generated from muscular tissue (it is called myalgia in
general but in reality myalgia is only one type of myogenous pain)
o Qualitative characteristics
§ Tenderness § Discomfort
§ Tightness § Muscle fatigue
- The protective co- contraction = muscle splinting = a response of the CNS injury or
the threat of injury
o NOT A MUSCULAR DISORDER just a clinical entity
o CONDITION OF THE MUSCLES THAT APPEARS OCCASIONALY
o Events responsible for protective co- contraction
§ Altered sensory or proprioceptive input
§ The presence of deep constant pain input
§ Increased emotional stress
o History reveals
§ A recent alteration in local structures
§ A recent source of constant deep pain
§ A recent increase in emotional stress
o Clinical characteristics
§ Dysfunction: decreased range of motion, but the pt can achieve a
relatively normal range when requested to do so (normal range of
motion is 40-55mm in max opening)
§ Min pain at rest
§ Increase of muscular pain during function (functional myalgia without
structural restraint)
§ Sense of muscular weakness
o Management: Resolve the issue that is responsible for the co- contraction,
and this action will normally resolve the protective co- contraction
immediately
- Reminder
o Polysynaptic reflex
§ Receptors
§ Sensory neurons (afferent n)
§ Interneurons
§ Motor neurons (efferent n)
§ Muscles
o Monosynaptic reflex
§ Receptors
§ Sensory neurons (afferent n)
§ Interneurons
§ Motor neurons (efferent n)
§ Muscles
- The most important reflexes on MS
o The myotatic (stretch) reflex = Jaw closing reflex = Jaw Jerk reflex
§ M contraction in response to stretching within the M
§ Monosynaptic reflex which provides automatic regulation of skeletal
M length
 § When a M lengthens, the M spindle is stretched and its nerve activity
increases
§ Responsible for the steady level of muscle tension, that is called
muscle tone

o Nociceptive (Flexor) reflex = Jaw opening reflex

§ The withdrawal reflex = a spinal reflex intended to protect the body
from damaging stimuli
§ The reflex rapidly coordinates the contractions of all the flexor M and
the relaxations of the extensors in that limb causing sudden withdrawl
from the potentially damaging stimulus
§ Spinal reflexes are often monosynaptic and are mediated by a simple
reflex arc
§ A withdrawal reflex is mediated by a polysynaptic reflex resulting in
the stimulation of many motor neurons in order to give a quick
response
§ Protects the M from a potentially damaging stimulus

- When an individual tries to chew

sth at the beginning the jaw closing reflex (Jaw Jerk/ myotatic r) is activated and
afterwards the jaw opening reflec (flexor reflex) is activated, if what is being chewed
can potentially harm the masticatory str
- Why stress affects the masticatory M? Why stress affects bruxism?
o Because of a phenomenon that is called gamma loop
o Be careful this is not flexor reflex
o When the limbic system is exposed to a stressor then the SNS (sympathetic)
is activated -> incr in adrenaline, nor- adrenaline and dopamine -> repeated
excitation of the limbic system happens under stress->
 o Afferent (sensory) neurons begin from the M spindle and go to the grey
matter of the spinal cord. There they create 2 synapses with gamma
(efferent) motor neurons. The first synapse has inhibitory action to the
antagonist M and the second synapse has excitatory action to the M that
contracted in the first place. Constant contractions of the M result in increase
of the M tone, because there is continuous feedback by the gamma efferent
neurons, that creates a loop
- Myogenous pain – clinical signs and symptoms
o Dysfunction: Limitation of jaw movements
§ Any effort to chew, speak, depress the mand increases the pain levels
o Acute malocclusion: Sudden change in the occlusal relationship between the
two dental arches
- Myogenous pain – aetiology
o Increased muscular activity +
o Vasoconstriction of the relevant arteries (ischaemia) +
o Accumulation of metabolic waste (lactic acid) +
o Release of algogenic substances = Myalgia
- Myalgia
o Pain worsens with jaw movement, function or parafunction
o Provocation test on the temporalis and masseter M replicates the pain
o Local pain -> it does not exceed the anatomic boundaries of the palpated M
o Possible pain locations: the jaw, the temple, in front of the ear duration of
pain: last 30d
- Myofascial pain
o Familiar myogenic pain
o Limitation of functional movements of the mandible
o Trigger points ***
o It may have a spreading behavior during palpation or it can be referral
o What are the trigger points? Firm, hypersensitive areas within the M that are
felt as bands or marbles in the muscular tissue during palpation
- Tendonitis
o Limitation of functional movements of the mandible, during function and
parafunction
o Provocation test on a muscular tendon replicates pain
o Any muscular tendon can be affected
o Most commonly affected tendon: temporalis tendon
o To diagnose tendonitis of the temporalis tendon: diagnosis of myalgia
restricted to the temporalis tendon
- Myositis (infective & non infective)
o Muscular pain (local myalgia) +
o Inflammation of the M +
o Infection of the M (not in non- infective myositis)
o Non infective
§ Chronic/ persistent local myalgia
§ Limitation of functional movements of the mandible
§ Appears as a manifestation of an autoimmune disease
§ Serologic tests reveal increased inflammation markers (CRP and ESR)
 § Implication: myositis ossificans -> calcification of the involved M (it
can also occur in infective traumatic myositis)
§ Not responsive to medication as infective myositis
§ Management: the med of the autoimmune disease. If myositis
ossificans occurs -> surgical exicision and physiotherapy
o Myositis ossificans
§ It is the heterotropic bone formation within a M
§ The anterior- posterior and lateral radiographs of the right elbow joint
showing distal ossification myositis of the right upper arm
§ A round mass sized about 5.53 cm x 4.10cm x 5.87cm was seen in
front of the distal humerus. MRI scan showed multiple cystic lesions
and mild bone marrow edema in the D humerus and ulna olecranon
§ CBCT scan showing calcification of the right medial pterygoid
o Infective
§ Acute appearance after trauma
§ Limitation on the mand movements
§ Infection signs = edema, erythema,
and/ or rise in temperature
§ Management: anti- inflammatory med
(NSAIDs) analgesics, antibiotics
- Spasm
o Spasm is the sudden, involuntary, reversible
tonic contraction of a M
o Clinical signs and symptoms
§ Immediate myalgia of any masticatory M
§ Immediate limitation of mandibular range of motion (max opening
<40mm, laterotrusion <7mm) sometimes acute malocclusion
o Management: reversable with relaxation techniques, TENS, injection of
anesthetic in the M
- Trismus
o Painful restriction of the mouth opening due to a M spasm that is induced
usually after a surgical procedure and/ or the injection of anesthetic. It is
suspected that it is either a toxic reaction to the anesthetic or an internal
hemorrhage of the M and sometimes there is also bacterial infection of the
affected M
o Clinical char: Limitation of functional movements + Spasm
o Management: Pharmaceutical (antibiotics, anti inflamm drugs NSAIDs) to
eliminate the bacterial factor. 2-4m time needed for symptoms to disappear
o IAN – never guide your needle inside the M
§ As long as you have guided correctly you do not need to have contact
with bone
- Other muscular conditions – Contracture
o It is the shortening of a M due to fibrosis of the tendons, ligaments or M
fibers
o History
§ Trauma, radiation therapy, infection
 § Also happens because the pt limits intentionally the extension of the
masticatory M
o Clinical char
§ Limitation of functional movements
§ Not painful
§ Pain occurs if during exam the examiner causes extension of the M
§ Prognosis: it is a reversible condition
o Management: high splints, physiotherapy, kinesiotherapy, if there was
infection then prescription of antibiotics and/ or anti- inflammatory drugs
needed
- Hypertrophy
o It is the enlargement of one or more masticatory M due to chronic tensing of
the M
o Clinical char: Obvious disfigure when it is unilateral
o Diagnosis: from photos and MRI
o Management: splints and BOTOX
- Neoplasm
o Based on there histologic char they are classified as
§ Benign (myoma)
§ Malignant (rhabdomyosarcoma/ metastatic tumor)
o Clinical characteristics: Swelling, spasm, pain at function, limitation of the
functional movements, sensory motor changes (paresthesia, hyperalgesia)
o Management
§ Depends on the results – excision of possible, radiotherapy, chemo
§ Always needs regular evaluation because this can affect other
masticatory str that due to meds or stress levels may develop TMD
L4: Lab prescription of medication
- Abbreviations
o tat = immediately o qty = quantity
o p.r.n. = pro re nata = when o Rx = prescription
required o Ref = refils
o o.d. – omni die = every day o q= every
o b.d. = bis die = twice a day o q4h= every 4 houts
o o.n. = omni die = every o qam = every morning
night o qhs= every night at
o t.d.s.= ter die sumendum = bedtime
to be taken three times o qid = 4 times a day
o q.d.s.= quarter die o qod = every other day
sumendum
- First producer – augmentin | Generic option = moxiclav
- 1st way – trade name
o Rx: Augmentin 500mg/ 125mg tabs, 1x3 (or tds)
o Sig: 1 tablet every 8 hours (or 1 tablets q8h)
nd
- 2 way = pharmaceutical substance, to allow the option of
generic drugs
o Rx: Amoxicillin/ Clavulanic acid 500mg/125mg tablets, 1x3
o Sig: 1 tablet every 8 hours
L5: Orofacial pain mechanism
- Pain = unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage
o Is pain and nociception the same thing? NO
§ Nociceptors are the nerves that detect noxious stimulu
and nociception is what they do for a living: they send reports about
tissue state, not pain
§ Pain is a brain- generated experience based on many factors,
including but not limited to nociception
o Mechanical nociceptors – detect sharp, pricking pain
o Thermal and mechano- thermal nociceptors – detects sensations which elicit
pain which is slow and burning or cold and sharp in nature
o Polymodal nociceptors – detects mechanical, thermal and chemical stimuli
- The nerve fiber
o Types and their char
o Which nerve fibers are excited with a painful stimulus?
§ Ad and C
- Reminder
o There are ascending (afferent n) and descending
(efferent n) neural pathways
§ Ascending -> from the receptor to CNS
(spinal cord/ brain)
§ Descending -> from the CNS to the organ/
tissue/ muscle/ effector in general
o The ascending tract
§ The impulse travels from the receptor to
the cerebral cortex. The impulse passes
through 3 neurons
• The 1st order neuron
• The 2nd order neuron
• The 3rd order neuron
§ Are the neurons actually in contact with each other? NO
• Neurotransmission – role of neurotransmitters
o Are endogenous chemicals that enable
neurotransmission
o type of a chemical messenger which transmits signals
across a chemical synapse, such as a neuromuscular
junction, from one neuron (n cell) to another ‘target’
neuron, M cell, or gland cell
• neurotransm inv in pain neural pathway
o The cause of stimulation may be internal, such as
pressure exerted by a tumor or external, for ex a burn.
o This noxious stimulation causes a release of chemical
mediators from the damaged cells including
§ Prostaglandin
§ Bradykinin
§ Serotonin
 § Substance P
§ Potassium
§ Histamine
§ Somatic Neural Pathway
• Painful stimulus – RECEPTOR ->
o 1st order neuron: the n gets in the spinal cord from the
post dorsal root and synapses with the 2nd order
neuron (at the same side where the stimulus occurred)
o 2nd order neuron: crosses over the opp site of the
spinal cord and gets in the spinothalamic tract. This
neuron ascends until it reaches the thalamus of the
brain, where it synapses with the 3rd order neuron
o 3rd order neuron carries the message to the respective
part of the somatosensory cortex that correlated with
the injured part of the body (the somatosensory cortex
at the opp site form the site where the receptor is
located). Perception of pain is accomplished at the
somatosensory cortex
• The neuron that are excited by the pain stumulus and the
neurons that are excited by a thermal stimulus (rise in
temperature), both enter the spinothalamic tract
• The neural pathway is also described as pain- temp neural
pathway
§ The nociception pathway (pain pathway) and the reflex arc neural
pathway that are excited by the same stimulus
o The descending pathway of pain – Endogenous opioids
§ Endorphins
• POMC
• B- endorphin, MSH, ACTH, LPH
§ Encephalins
• Preproencephalin
• Leu & Met Encephalin
§ Dynorphins
• Preprodynorphin
• Dynorphin A & B
o What happens at modulation of pain?
§ Neurotransmitters from the descending
pathway of pain that act on the ascending
pathway, by occupying the receptors that
normally should be occupied by
neurotransmitters responsible for the
transmission of pain. The neurotransmitters have inhibiting action on
the transmission of pain
§ The red dots represent a neurotransmitter of the ascending pathway
of pain that promotes the transmission of pain to the CNS until it
reaches the cortex where the pain becomes a conscious experience
 o Endogenous opioids= encephalins and endorphins that are primarily
produced in the brain and have multiple actions throughout the body.
Encephalins and endorphins act at opioid receptors and their activity can be
clocked by opioid antagonists
§ The human body naturally produces its own opiate- like substances
and uses them as neurotransmitters. These substances include
endorphins, encephalins and synorphin, often collectively known as
endogenous opioids. Endogenous opioids modulate our reactions to
painful stimuli
o Explaining the descending pathway of pain
§ In the descending pathway of pain the efferent neurons follow a path
through which they trigger production and release of endogenous
opioids. The endogenous opioids are released in the descending
pathway and their amount is enough to reach and target the
neighbouring ascending neurons of the ascending pathway, where
they block the neurotransmission that prostaglandins (or other pain
neurotransmitters) do, to interrupt the transmission of pain to the
cortex. The encephalins have inhibitory action on the
neurotransmission of pain because they occupy the receptors that
normally would be occupied by the prostaglandins. The modulation
begins after the pain message has reached at least once the cortex
- What are the 4 stages of pain
o Transduction: Begins when the free n endings
(nociceptors) of C fibers and A-delta fibres of primary
afferent neurons respond to noxious stimuli.
Nociceptors are exposed to noxious stimuli when
tissue damage and inflammation occurs as a result
of, for example, trauma, surgery, inflammation,
infection and ischaemia
o Transmission: Occurs in 3 stages. The pain impulse is
transmitted
§ From the site of transduction along the nociceptor fibres to the dorsal
horn in the spinal cord
§ From the spinal cord to the brain stem
§ Through connections between the thalamus, cortex and higher levels
of the brain
o Perception = end result of the neuronal activity of pain transmission and
where pain becomes a conscious multidimensional experience. The
multidimensional experience of pain has affective- motivational, sensory-
discriminative, emotional and behavioral components
§ When the painful stimuli are transmitted to the brain stem and
thalamus, multiple cortical areas are activated and responses are
elicited
o Modulation: Involves changing or inhibiting transmission of pain impulses in
the spinal cord. The multiple, complex pathways involved in the modulation
of pain are referred to as the descending modulatory pain pathways (DMPP)
 and these can lead to either an increase in the transmission of pain impulses
(excitatory) or a decrease in transmission (inhibition)
§ Descending inhibition involves the release of inhibitory
neurotransmitters that block or partially block the transmission of
pain impulses, and therefore produce analgesia
- Orofacial pain: The pain that originates from oral str accompanied by facial pain. The
facial area includes the region demarcated as below the orbitomeatal line, above the
neck and anterior to the ears
o Do the mechanisms of the somatic pain neural pathway apply in orofacial
pain?
§ YES BUT with several differences
o Which neural fibres are involved in this pathway?
§ Adelta and C
o Trigeminal nerve (CNV)
§ What is a ganglion?
• A ganglion is a nerve cell cluster or a
group of nerve cell bodies located in the autonomic nervous
system and sensory system. Ganglia house the cell bodies of
afferent n and efferent n
• Gasserian ganglion: The trigeminal ganglion (or Gasserian
ganglion, or semilunar ganglion or Gasser’s ganglion) = sensory
ganglion of trigeminal n (CNV) that occupies a cavity (Meckel’s
cave) in the dura mater, covering the trigeminal impression
near the apex of the petrous part of the temporal bone
§ The mandibular n originates from the trigeminal n (CNV), specifically
the trigeminal ganglion. The mesencephalic nucleus is important for
proprioception related to the M innervated by the mandibular n, but
it is not the origin of the n itself
§ The nuclei in the brainstem are clusters of neurons that perform
essential functions related to both sensory and motor processing. The
brainstem consists of the midbrain, pons and medulla oblongata and
within these areas, various nuclei ctrl vital functions such as
breathing, heart rate, movement and sensory processing. The specific
functions of the nuclei in the brainstem depend on their location and
the type of neurons they contain (sensory, motor or mixed)
o Motor nuclei of the cranial n - These include nuclei responsible for motor
functions of the CN such as
§ Oculomotor nucleus (CNIII) – controls eye movement
§ Trochlear Nucleus (CNIV) – ctrls the sup oblique M (eye movement)
§ Abducent nucleus (CNVI) – controls the lateral rectus M (eye
movement)
§ Trigeminal motor nucleus (CNV) – ctrls the M of mastication (chewing)
§ Facial nucleus (CNVII) – ctrls facial expression M
§ Nucleus ambiguous (CNIX, X) – ctrls M involved in swallowing and
speech. Hypoglossal nucleus (CNXIII) – ctrls tongue movement
 o Sensory nuclei: These nuclei process sensory info (such as pain, temperature,
touch and proprioception) from the head and neck and send this info to the
higher parts of the brain for processing
§ Trigeminal sensory nucleus (CNV) – divided into 3 parts
• Mesencephalic nucleus – processes proprioceptive info from
M of mastication (jaw position and movement)
• Principal sensory nucleus – processes touch and pressure
sensations from the face
• Spinal trigeminal nucleus – processes pain and temperature
sensations from the face
§ Nucleus of the solitary tract: receives sensory info related to taste and
visceral sensations (e.g. from the internal organs). It is responsible for
taste sensations via CNVII, IX and X
§ Cochlear and Vestibular nuclei (CNVIII): these nuclei are involved in
hearing and balance. The cochlear nuclei process auditory info, while
the vestibular nuclei are responsible for balance and spatial
orientation
o Damage of trigeminal
§ Increased sensation of pain
§ Decreased sensation of apin
§ Paralysis of the masticatory M
§ Neuralgia (neuropathic pain)
- Orofacial pain
o The ventral trigeminothalamic tract carries pain and temperature sensaitons
from the face and the oral cavity
o The dorsal trigminothalamic tract carries sensations of tactile discrimination
and pressure from face and oral cavity
o The oral cavity has bilateral sensory projections, whereas other facial str have
only contralateral sensory projections
- Contralateral sensory projections vs Bilateral
o Bilateral sensory projections (oral cavity): Bilateral means that sensory
information from the oral cavity (including the tongue, lips, and mouth) is
sent to both sides (left and right) of the brain. This means that sensory input
(such as touch, pain, or temperature) from the left side of the oral cavity is
processed by both the left and right sides of the brain, and the same happens
for the right side of the oral cavity. This bilateral processing allows for more
coordinated control and response to sensations in the mouth. For example, if
something touches the left side of your tongue or if you have a painful
sensation in the mouth, both sides of your brain are involved in processing
and responding to that information.
o Contralateral (other facial str): Contralateral means that sensory information
from other facial structures (like the skin on your face, eyes, or nose) is sent
to the opposite side of the brain. For instance, if the left side of your face is
touched, the sensory information is relayed to the right side of the brain.
Similarly, sensory input from the right side of your face would be processed
by the left side of the brain. This contralateral projection is typical of sensory
 pathways, such as the somatosensory system, which generally crosses over
to the opposite side of the brain at the level of the brainstem.
- The neural pathway of orofacial pain
o The bilateral projection of the oral cavity may have evolved to provide
redundant processing for such a sensitive and important area. Since the
mouth is involved in essential functions like eating, speaking, and breathing,
having sensory input processed on both sides of the brain might help in faster
and more coordinated responses to stimuli. On the other hand, contralateral
projection in most other facial structures (like the skin of the face) is more
typical of sensory pathways, where one side of the body sends its sensory
input to the opposite hemisphere of the brain for processing.
o In summary
§ Oral cavity – sensory info from the oral cavity (e.g. lips, tongue) is
processed by both sides of the brain (bilaterally)
§ Other facial structures – sensory info from other parts of the face
(skin) is processed by the opposite side of the brain (contralaterally)
- Classification of orofacial pain
o Orofacial pain attributed to disorders of dentoalveolar and anatomically
related str
o Myofascial orofacial pain
o TMJ pain
o Orofacial pain attributed to lesion or
decrease of the CN
o Orofacial pains resembling presentations of
primary headaches
o Idiopathic orofacial pain
- Gate ctrl theory of pain
o The Aβ and C fibres transmit their impulse with a certain velocity .
o Their transmission can be interrupted if excitation of neighbouring fibres (ie.
Aβ- motion) occurs, that transfer their own impulse with higher velocity
(reminder: the bigger the diameter of a nerve fibre,the higher the
transmission velocity)
o The impulse that is transferred by other-quicker nerve fibres- interrupts the
impulse of the Aδ and C fibres, and it is ‘closing the gate of pain’
o TENS

L6: Disc condyle disorders

- Types of sounds recorded during examination
o Expected normal sounds
o Clicking (normal/ abnormal) -> POPPING sound
o Crepitus -> egg- shell- cracking sound, walking
on the sand sound
- Types of TMJ sounds
o Normal/ expected
o Crepitus
o No sound/ DdwtR
o Clicking = Anatomical, Hypermobility, Asynchronicity, DdwR
- Crepitus
o Like walking on snow or thick sand
o It indicated that there is structural
degenerative deformity of the osseous
structures and perforation or destruction
of the articular disc
o The sound is a result of the friction
o Expected: in old people (degeneration due
to ageing) and patients that have
removable dentures
o Not expected: in young people, but needs
investigation
- Degenerative intra- articular lesions
o Disc perforation = arthritis
o Crepitus = distinctive intra- articular sound of degeneration
- Clicking
o Clicking sound attributed to structures that are deformed but not
degenerated
§ These clicking sounds are a result of
a deformation during body
development or a result of the
remodelling of the structures of the
joint due to the loads of forces acted
on the TMJ
o Clicking due to hypermobility
§ This sound is produced when the condyle
jumps over and skips the articular
eminence slightly. A condition that is
expected in individuals that are hyper-
flexible
§ This is NOT a TMJ luxation, it is a
subluxation (it is not a joint dislocation)
§ Condyles skip the artic eminence at max opening
§ Normal ability in opening and closing movements, but at the end of
the opening movement there is a clicking sound and deviation at the
opposite site. The closing movement does not produce any sound
o Clicking attributed to muscular asynchronicity
§ The two heads of the lateral pterygoid muscle normally have
competitive action; the upper head is activated during the opening
movement and the lower head during the closing movement. If they
remain synchronized there is a stable movement of the condyle and
the articular disc can obtain a fixed position at the closing of the
mouth BUT… If the two heads are
asynchronized -> asynchronized movement
of the disc-> multiple clicking sounds that
are not always at the same level at both
opening and closing movements
 o Clicking due to muscular asynchronicity
§ Diff types of opening patterns that can be
recorder even on the same appointment in
the same pt. the cross indicates the level that
you notice the sound. The multiple clicking
sounds come from the affected joint. For this
example, we consider that the right joint is
the affected.
o Clicking attributed to disc displacement with reduction
§ At the beginning of the opening movement the disc is pushed at the
front and the ligaments that are attached to it posteriorly are
stretched. The clicking sound is produced when the condyle jumps
over the disc abruptly. After the clicking sound the patient can
perform the opening movement normally. At the closing movement-
close the end of the movement – there
is clicking sound again
§ For this example, consider that the first
cross on the top indicated a clicking on
the right TMJ, and the second one
indicates a clicking on the left TMJ
- Locking/ Disc displacement without reduction
o The disc is permanently displaced at the
front (usually)
o Clinically: limited opening of the mouth (at
the close lock), NO SOUND, and deviation
of the mandible ipsilaterally (to the side
where the disc is dislocated)
o The open lock and close lock
§ Open lock
• In close mouth position the
disc in an anterior position
relative to the condyle
• Medial or lateral disc displacement is also possible
• Clinical observations:
o At opening: uncorrected deviation at the affected side,
NO limitation of jaw opening (at max assisted opening
at least 40mm)
o Lateral movement to the opp side is impossible
§ Close lock
• In close mouth position the disc is in an anterior position
relative to the condyle
• Medial or lateral disc displacement is also possible
• Clinical observations:
o At opening: uncorrected deviation at the affected side,
limited jaw opening severe enough to interfere with
the ability to eat
o Lateral movement to the opp side is impossible
 - The endfeel test = maximum assisted opening = passive stretch
o This is a test performed by the clinician to distinguish the locking from the
muscular disorders
o At locking the maximum unassisted opening and the maximum assisted
opening give the same measurement
o At muscular disorders usually the max assisted opening is slightly increased
compared to the maximum unassisted opening
o Performed by the clinician
- Disc condyle discorders
o Disc displacement with reduction
o Disc displacement with reduction with intermittent locking
o Disc displacement without reduction with limited opening (= close lock)
o Disc displacement without reduction without limited opening (= open lock)
- Hypomobility disorders
o Adhesion/ adherence
§ Cause: fibrotic changes to capsular ligaments
§ Clinically:
• Restricted mandibular movement
• Deflection to the affected side on opening
o Ankylosis
§ Cause: formation of a bony mass that causes the fusion of the other
components of the joint
§ Clinically:
• Limited range of motion
• Deflection to the affected side
• Limited laterotrusion to the contralateral side
- Hypermobility disorders
o Subluxation
§ Disc condyle complex is placed anterior to the articular eminence and
can be repositioned in the fossa only with a maneuvre by the pat
§ Clinically:
• Inability to close from the wide opening position at least the
last 30 days
• Mouth closing is achieved only with manual manipulation by
the pt
o Luxation Also called open lock
§ Disc- condyle complex is placed anterior to the articular eminence and
can be repositioned in the fossa only with a maneuvre by the clinician
§ Clinically:
• The mouth is wide open or the jaw is protruded
• Mouth closing is achieved only with manual manipulation by
the clinician

L7: Osteoarthritis
- Osteoarthritis = mentioned scientifically = erosive osteoarthritis
o Most common type of arthritis
o Amongst the 10 diseases that cause disability
 o People working in agriculture for
§ 1-9 ages -> p= 4,5 times higher risk
§ >10 ages -> p=9,3 times higher risk
§ 80% of the diagnosed individuals have limited mobility and the 25% of
the diagnosed and/ or weakness in accomplishing simple daily tasks
- RA, JA, PA -> SYSTEMIC arhtritides
o All of them belong to the group of systemic arthritides and ALL of them are
considered inflammatory arthritides
o OA = NOT an autoimmune disease
- Types of arthritides
o Inflammatory (autoimmune)
§ RA
§ PA
§ JA
o Non inflammatory
§ OA
- What is OA and where is this disease attributed to?
o = a degenerative joint disease, which mainly affects the articular cartilage. It
is associated with ageing and will most likely affect the joints that have been
continually stressed throughout the years including the knees, hips, fingers
and lower spine region
o The knee is usually the first joint to be affected
o While osteoarthritis is a degenerative joint disease that may cause gross
cartilage loss and morphological damage to other joint tissues, more subtle
biochemical changes occur in the earliest stages of osteoarthritis progression.
The water content of healthy cartilage is finely balanced by compressive
force driving water out and hydrostatic and osmotic pressure drawing water
in. Collagen fibres exert the compressive force, whereas the Gibbs–Donnan
effect and cartilage proteoglycans create osmotic pressure which tends to
draw water in. However, during onset of osteoarthritis, the collagen matrix
becomes more disorganized and there is a decrease in proteoglycan content
within cartilage. The breakdown of collagen fibers results in a net increase in
water content. This increase occurs because whilst there is an overall loss of
proteoglycans (and thus a decreased osmotic pull), it is outweighed by a loss
of collagen. Without the protective effects of the proteoglycans, the collagen
fibers of the cartilage can become susceptible to degradation and thus
exacerbate the degeneration. Inflammation of the synovium (joint cavity
lining) and the surrounding joint capsule can also occur, though often mild
(compared to the synovial inflammation that
occurs in rheumatoid arthritis). This can
happen as breakdown products from the
cartilage are released into the synovial
space, and the cells lining the joint attempt
to remove them.[citation needed]
o Other structures within the joint can also be
affected. The ligaments within the joint
become thickened and fibrotic and the
 menisci can become damaged and wear away. Menisci can be completely
absent by the time a person undergoes a joint replacement. New bone
outgrowths, called "spurs" or osteophytes, can form on the margins of the
joints, possibly in an attempt to improve the congruence of the articular
cartilage surfaces in the absence of the menisci. The subchondral bone
volume increases and becomes less mineralized (hypomineralization). All
these changes can cause problems functioning. The pain in an osteoarthritic
joint has been related to thickened synovium and subchondral bone lesions.
- Evolution of OA
- Risk factors for OA
o Age- ageing of the joint tissues
§ Primary OA
o Increased loads in the joints (from physical
activity, excessive activity, obesity)
o Trauma
o Family history
o Autoimmune disease
o Joint deformity such as unequal leg length, bowlegs or knocked knees
§ Secondary OA
- Stages of progression in OA
- Management of OA
o Non pharmacologic
§ Splint on the affected joint
§ Exercise
§ Weight loss
§ Neuromuscular balancing
§ Physiotherapy (TENS, iontophoresis, ultrasound- therapeutic heat)
§ Topical capsaicin
o Pharmacologic
§ Analgesics § Intra- articular
§ Acetaminophen corticosteroids
§ NSAIDs § Intra- articular
§ Glycosamine anesthetic
§ Chondroitin § BOTOX
§ Bisphosphonates
- Management of TMJ OA
o Non pharmacologic
§ Splint
§ Physiotherapy (TENS, iontophoresis, ultrasound- therapeutic heat)
§ Kinesiotherapy for muscular balancing
o Pharmacologic
§ Analgesics (pain killers)
§ Either only paracetamol or in combination with codeine
§ Acetaminophen
§ NSAIDs
§ Glycosamine
§ Chondroitin
 § Bisphosphonates – only if there are many joints affected
§ Intra- articular corticosteroids
§ Intra- articular anesthetic
§ BOTOX
- OA vs RA
o OA: Degenerative disease, morning stiffness lasting less than 30mins,
cartilage loss, heberden’s nodes, asymmetrical
o RA: autoimmune disease, morning stiffness lasting more than 30 mins,
inflamed synovium, extra articular involvement, symmetrical
- How do we set the diagnosis of OA?
o History +
o Clinical exam +
o Radiographic imaging
o = diagnosis of OA
o Symptoms: joint stiffness, pain, limitation in
the range of motion, joint swelling, crepitus
- Radiographic evidence of TMJ OA
o Decrease in joint space- non uniform joint
space loss
o Flattening of the condyle surface
o Perforation of the periosteum (erosive subchondral erosion)
o Osteophyte formation (spurs)
o Cyst formation
o Subchondral sclerosis
- Radiographic evidence of knee OA - 2 classification systems of the radiographic
findings for knee OA
o Ahlback system = comments on the changes in the intra- articular space
o Kellgran & Lawrence system = comments on the intra- articular space,
appearance of spurs and sclerosis
- Classif systems for knee OA
o Kellgren and Lawrence system
§ 0: no radiographic features of OA are
present
§ 1: doubtful joint space narrowing (JSN) and
possible osteophytic lipping
§ 2: definite osteophytes and possible JSN on
anteroposterior weight-bearing radiograph
§ 3: multiple osteophytes, definite JSN,
sclerosis, possible bony deformity
§ 4: large osteophytes, marked JSN, severe
sclerosis and definite bony deformity
o Ahlback
§ Grade 1= joint space narrowing (less than 3mm)
§ Grade 2= joint space obliteration
§ Grade 3 = minor bone attrition (0-5mm)
§ Grade 4 = moderate bone attrition (5-10mm)
§ Grade 5 = severe bone attrition (more than 10mm)
- Clinical evidence of OA in other joints
o Bouchard nodes = bony swelling of the proximal interphalangeal joint
o Haberden nodes = bony swelling of a distal interphalangeal joint
- Comments about TMJ OA
o It is possible to have patients with TMJ OA only and no other joint in their
body is affected. It is also possible that the first time they begin experiencing
the symptoms in full range will be when the OA has severely progressed.
o This is common in bruxers and patients that have lost to many posterior
teeth and did not proceed in restoring the missing teeth.
o A complete treatment approach of a TMJ OA includes management of the
pain episodes and the relapses, and when the condition is in remission the
restoration of the dentition (if needed)
o A hard stabilization splint supports the affected joints and releases the forces
that create the loading. Since the initial stages of OA are not inflammatory,
the pain can be managed by analgesics.
- What is osteoarthrosis?
o In the past there was use of the term osteoarthrosis that meant degeneration
of the joint without signs of inflammation. The patient was not experiencing
relapses during which he could be in severe pain
o Term was used to show that the patient was experiencing symptoms that
were indicative of inflammation
o Today, we know that the osteoarthrosis is the primary osteoarthrosis that
appears in elderly patients and the level pain episodes is subjective and sth
that each patient experiences individually. The inflammation symptoms are
mild and usually appear when the osteoarthritis progresses severely
- Osteophyte (bone spur) = bony outgrowth that forms along the edges of bones,
particularly at joints or where tendons and ligaments attach to bones
- Subcortical/ subchondral cyst
o A subcortical cyst in osteoarthritis (OA) refers to a fluid- filled cavity that
forms within the subchondral bone—the layer of bone just beneath the
cartilage in a joint.
o These cysts are commonly observed in OA and are considered a marker of
disease progression.
o It is suggested that there are two possible mechanisms for their formation
§ [Link] Fluid Intrusion: A breach in the subchondral plate allows
synovial fluid to enter, leading to cyst formation. (PubMed)
§ [Link] Microfractures: Mechanical stress from cartilage loss causes
microfractures in the subchondral bone, initiating cyst
development.(PubMed)
o These cysts are often accompanied by increased bone turnover, including
higher numbers of osteoclasts bone-resorbing cells) and osteoblasts (bone-
forming cells), indicating active bone remodelling. OARS JOURNAL
o The term "subcortical“ or subchondral denotes the bone layer beneath the
cartilage, while "sclerosis" indicates an abnormal increase in bone density. In
OA, subcortical sclerosis arises as a response to altered mechanical stress on
the joint. Over time, this leads to increased bone formation and
 mineralization in the subchondral region, which is visible on X-rays as areas of
increased density .
o Subcortical sclerosis is thought to result from microfractures in the
subchondral bone due to abnormal joint loading. The body attempts to repair
these microfractures by increasing bone density, leading to sclerosis. This
process may occur before significant cartilage damage becomes apparent,
suggesting that subcortical sclerosis could play a role in the early stages of OA
- Ankylosis of the TMJ = a condition where the jawbone becomes fused to the skull
due to bony or fibrous tissue, leading to limited mouth opening and potential facial
deformities. This condition can significantly impact funcitons like chewing, speaking
and maintaining oral hygiene
o A modified classification system categorizes TMJ ankylosis into 4 types
§ Type I: non- bony ankylosis with almost normal- joint space
§ Type II: lateral bony ankylosis with a normal joint space and a
radiolucent line
§ Type III: complete bony ankylosis with only a radiolucent line
§ Type IV: extensive bony ankylosis without any radiolucent line
o Younger trauma patients tend to develop more severe types, and longer
post- trauma periods are associated with more severe ankylosis

L8: Bruxism
- Definition
o Bruxism: The parafunctional grinding of teeth
§ An oral habit consisting of involuntary rhuthmic or spasmodic
nonfunctional gnashing, grinding, or clenching of teeth, in other than
chewing movements of the mandible, which may lead to occlusal
trauma; comp, nocturnal bruxism, occlusal necrosis, tooth grinding
§ A sleep related movement disorder
§ Diurnal or nocturnal parafunctional activity including clenching,
bracing, gnashing and grinding of the teeth
§ The need to have independent definitions for diurnal and nochturnal
bruxism
§ Sleep bruxism = masticatory M activity during sleep that is
characterized as rhythmic (phasic) or non- rhythmic (tonic) and it is
not a movement disorder or a sleep disorder in otherwise healthy
individuals
§ AB = multifactorial etiology, central mechanisms inv
§ Awake bruxism = masticatory M activity during wakefulness that is
char by repetitive or sustained tooth contact and/ or by bracing or
thrusting of the mandible and it is not a movement disorder in
otherwise healthy individuals
§ AB = mainly tic or habit or parafunction
o Bruxomania: Grinding of teeth occurring as a neurotic habit the waking state
o Awake bruxism – diurnal
o Sleep bruxism – nocturnal
- International consensus on the assessment of bruxism
o Diagnosis based on
 § History and personal report
§ Clinical exam
§ Electromyographic activity
§ Polysomnography (GOLDEN standard)
o Classif of bruxism based on the impact on health
§ Harmful
§ Risk factor
§ Protective factor
- Classif of bruxism based on its characteristics
o Based on time of occurrence
§ Nochturnal
§ Diurnal
o Based on aetiology
§ Primary
§ Secondary
o Based on EMG activity
§ Phasic (at least 3 EMG bursts 0,25 secs – 2 secs)
§ Tonic (1 EMG burst, >2 secs)
§ Combined
- Aetiology of SB = multifactorial
o Primary SB
§ Microarousals + RMMA
§ Stress
§ Genetics
§ Personality traits
o Secondary SB
§ Comorbidity
§ Drug induced SB
- Primary sleep bruxism vs Secondary sleep bruxism
o SB is classified as primary when no clear medical cause is present(also called
idiopathic). Aetiology of most SB cases is primary. SB is classified as
secondary when it is a comorbidity or when it is caused by a clinical,
neurological or psychiatric disorder, use or suppression of substances or
medications, or when it is associated with another primary sleep disorder.
- Microarousal + RMMAs
o Microarousal: it begins with the rise in autonomic cardiac activity and ends at
the point where the muscular tone of the depressor muscle increases
o RMMA- Rhythmic Masticatory Muscle Activity: it is the electromyographic
activity of masticatory muscles that appear as EMG bursts. Any burst during
sleep is considered a bruxing event when this is at least 1/10 of the EMG
activity recorded at an intentional maximum bite force
- Stress
o Indexes to estimate the stress levels
§ Catecholamines in urine: Adrenaline, noradrenaline, dopamine
§ Chromogranin A in saliva (CgA)
• Appears to be more sensitive to emotional stress and not
other body stressors
 o The gamma loop biofeedback
§ Be careful,this is not the flexor reflex!!!
§ When the limbic system is exposed to a stressor then the
SNS(sympathetic nervous system) is activated => increase in
adrenaline, nor-adrenaline and dopamine=> repeated excitation of
the limbic system happens under stress=> a afferent (sensory)
neurons begin from the muscle spindle and go the grey matter of the
spinal cord. There, they create 2 synapses with γ (efferent) motor
neurons. The first synapse has inhibitory action to the antagonist
muscle and the second synapse has excitory action to the muscle that
contracted in the first place. Constant contractions of the muscles
result in increase of the muscle tone, because there is continuous
feedback by the γ efferent neurons, that creates a loop.
• Limbic system = part of the brain involved in our behavioral
and emotional responses
- Personality traits: People with anxiety, daily stress and a tendency to perfectionism,
or the tendency to seek reassurance appear to have poor coping mechanisms or
sometimes they develop malfunctional coping mechanisms that make them
susceptible in manifesting bruxism
- Drug induced bruxism
o There are meds and chemical substances that at certain doses- usually high –
appear to increase the muscular activity of the masticatory M
o Selective reuptake inhibitor antidepressants
o Calcium channel blockers (flunarizine)
o Antidopaminergic drugs
o Antipsychotics (dopamine neurotransmission antagonists)
o Amphetamines, ecstasy
o Caffeine
o Cocaine
o Tobacco
- Comorbidity
o Assoc with sleep disorders
§ Restless legs syndrome
§ REM sleep behavior disorder
§ Obstructive sleep apnea – hypoapnea
o Neurologic disorders
§ Huntington’s § Myofascial pain
disease § Mental retardation
§ Hemifacial spasm § Attention deficit-
§ Parkinson’s hyperactivity
§ Demencies disorder
§ Multiple system § Rett syndrome
atrophy § Comatose state
§ Gilles de la Tourette § Post- anoxia
syndrome encephalopathy
§ Cerebellar vascular
accident
 o Psychiatric disorders
§ Schizophrenia
§ Affective disorders
§ Nervous bulimia- nervous anorexy
o Other diseases
§ Xerostomy
§ Gastroesophageal reflux
§ Sjogrens
- Genetics
o Is there a gen or genetic index to which bruxism is attributed? No
§ But the knowledge we obtained from clinical studies suggests a
contribution of genetic background
o How do we know that genetics contribute?
§ Expression of the similar bruxing characteristics amongst relatives
(similar shape of bruxing facets and sometimes similar teeth affected)
- Is bruxism always harmful?
o No it is not. There is a theory that refers to obstructive sleep apnea
o Apnea is a serious condition that can cause death
o If the patient experiences apnea during sleep and the levels of oxygen drop
dramatically, the CNS triggers the RMMA to force the masticatory structures
to open the mouth and let air get into the respiratory tract.
- Can occlusion cause bruxism?
o NO occlusion cannot cause bruxism and it is not considered a primary factor
aetiologically.
o BUT malocclusion or occlusal interferences can contribute in the aggravation
of the symptoms of a bruxer. Occlusal interferences may induce awake
bruxing as a tic to eliminate the interference(for example after a restoration
where the occlusion was not checked properly).
o How do we know?
§ There are individuals with naturally close- to- ideal occlusions that are
bruxers
§ There are bruxers that had occlusal therapies (orthodontics,
phonetics) for the treatment of bruxism that are unsuccessful
§ There are individuals with adequate occlusions or malocclusion that
are not bruxers
- Diagnosis – Impact on the S.S.
o Teeth
§ Tooth wear
§ Bruxing facets
§ Root absorption
o Muscles
§ Myalgia or other types of muscular
orofacial pain
§ Muscular hypertrophy
o Joints
§ Disc condyle complex disorders
§ Arthralgia
 § Osteoarthritis
- Masseteric hypertrophy
- Treatment approach – Is there a treatment? No there is no. we manage each relapse
accordingly, mostly with non pharmaceutical means and rarely with pharmaceutical
means. The approach is management NOT a permanent treatment, and the patients
must know that they will have to live with this approach for the rest of their lives
o Non pharmaceutical
§ Splints
• Hard (not soft) that promote expansion of the M
• To protect the dentition
• To protect the TMJS from excessive loads
§ Physiotherapy
• It is used to relief pain and relax the M of the SS
• The pain relief is based on the Gate Control theory of pain
§ Psychotherapy
• It is used to resolve stress issues and to help the patient
release the stress levels and anxiety
• It is also used to manage the behavioral issues in diurnal
bruxism
§ Pharmaceutical
• Muscle relaxants
• Dopaminergic agonists Levodopa (L- Dopa)
• Diazepam
• Benzodiazepines
§ BOTOX
• Type A (7 types overall)
• Botilinum toxin coming from the bacteria Clostridium
Botulinum => paralyses the M. it is used to decrease muscular
activity. The result lasts from several weeks to several months
depending on the dose
• Indications
o Muscular hypertrophy
o After several months to a year of failed conservative
approach
o Orofacial dystonia
• Failure = not even one period of remission, or no decrease in
pain level with other means
• There is not enough evidence of its effectiveness or impact
long- term, that is why it is used only as a last option
- Bruxism in childhood
o It is considered an expected condition as long it does not progress into a TMD
o Self- limited as the permanent dentition replaces all the deciduous teeth
o Usually if bruxing episodes do not subside after adolescence, then we expect
repeated reoccurences
L9: Management of TMD – Different types of splints
- Management of TMDs
o Goals
§ Decrease pain
§ Decrease adverse loading
§ Restoration of function
§ Resumption of daily activities
o The plan is to treat/ manage the physical disorders and reduce/ eliminate the
effects of the contributing factors
o Before management

o After management

o Reasons of unresponsive conservative therapy of a TMD

§ Incomplete/ incorrect diagnosis
§ Unsuccessfully addressed/ unrecognized contributing factors: in
chronic orofacial pain conditions there has to be contribution of
specialists from different fields (neurologist, psychiatrist, psychologist,
rheumatologist, anesthesiologist, gnathologist etc)
o reversible
§ pt education & self-management – Biobehavioral therapy
• the success dep more on the pt and less on the clinician
• key part = Clinician’s explanation of the problem
• MOTIVATION + COOPERATION + COMPLIANCE = SUCCESS
• Parafuncitonal habit reversal!!!
• Common parafunctional habits – clenching, bruxing, tongue,
thrusting, cheek biting, poor sleep posture, object biting
§ orthopedic appliances (splints)
• How do they work?
o O disengagement – temporary cancellation of the
existing O contacts
o Changes the VDO because the splint’s height is added
o Changes of the relationship between condyle and
glenoid fossa
o Decreased loading of all the str of the SS
o Neurophysiological changes
o Behavioral changes
o Placebo effect
• Stabilization splint = occlusal splint = Michigan splint
o MOST common used type of splint
 o Height varies -> dep on the diagnosis
o Hard & flattened O that provide full coverage
o Can be placed either on the mandible or the maxilla
o Indications
§ Acute/ chronic symptoms on the teeth/ Mastic
M/ TMJS attributed to a TMD
§ Bruxism -> to avoid tooth wear/ worsening the
tooth wear and aggravation of intra- articular
disorders (disc displacement with/ without
reduction, degen due to loading)
o Anterior guidance = about 18mm
o It is not necessary to have contacts everywhere, as long
as the contacts are balanced and they do not disturb
the occlusal surface of the splint to the point that this
changes the occlusal scheme
• Shore plate: It is an altered stabilization splint that is extended
to the palate. The palatal part is extremely smooth. The splint
is stable because of metallic rings that hug the first upper
molars
o Indications
§ TMDs attributed to tongue thrusting
§ Abnormal overjet (increased overjet)
§ Abnormal overbite
§ Daily use in pts with disc lock
• Anterior repositioning splint/ Farrar’s splint = This splint has
an anterior part with inclination
o Indication: anterior disc displacement with reduction
o Theory behind it = The condyle is placed in a new
position anteriorly, where the relationship to the disc is
different than previously and the clicking sound is
avoided
o Results = doubtful
o At the beginning the clicking stops but then it returns
o There is overstretch of the disc ligaments, and the
clicking returns even in the new position
• Anterior bite splint (the anterior deprogrammer)
o Indication: immediate/ fast deprogramming
(relaxation) of the masticatory M -> ex: at extensive
restorations that include long appt, at the point that
we need to record the bite registration we may get an
incorrect bite because the M are tired. At this point we
fabricate a deprogrammer and wait for the M to relax
o It has partial coverage
o Cannot be used long term bec it can cause over
eruption (max 2 w)
• Athletic splint
 o Indication: a sport that has a possible harmful impact
on the str of the SS (football, basketball, karate, tae
kwon do, boxing, ice hockey etc)
o Functions of athletic splint
§ Dental protection
§ Soft tissue protection
§ Concussion protection
§ Bone protection
§ TMJ protection
o With the athletic splints we tend to improvise based on
the need of protection for each sport
o Athletic splints are considered ‘soft splints’ and the
most comm used material is EVA (ethylene vinyl
acetate). In general there are different polymeric and
thermoformable materials referred in literature and
these are
§ Polyvinyl chloride
§ Acrylic resin
§ Polyurethane
§ Polyolefin
§ Latex rubber
o The impact tests for athletic mouthguards and the
materials they are made of are testing
§ The absorption of impact forces
§ The distribution of forces
o REMEMBER! The level of protection may vary per
sport! Principles of fabricating an athletic splint
§ The thickness of the material used should be at
least 4mm in the important impact zones (ant
teeth, alv bone at the M)
§ Bite registration is better to be recorded at the
position the pt is intending to use the splint
§ Coverage: full coverage of the upper arch
§ Margins: all the teeth of the respective arch are
covered with the material, plus as much of the
alveolar bone as possible, dep on how much
coverage this athlete can handle
§ The O surface has the -ve imprint of the
opposed arch it is not flattened as the
stabilization splint
• Soft or hard splint?
• Soft splints - NEVER AIMED TO TREAT TMD – ATHLETIC OR
WHITENING
o Not as effective in muscular disorders and intra-
articular disorders
o Easily damaged and perforated from bruxing activity
 o Clinical researches that show some effectiveness of
soft splints, but until now it remains doubtful, and it is
suspected that his might be a placebo effect
• Hard splints (heat cured acrylic)- Appear to deliver results
sooner and they provide long- term stability of all the str of
the SS
o Maintain a stable distance between the condyle and
the glenoid fossa
o Prevent the extension of tooth wear
o Force the M to relax sooner
o Train the pt to realize the obtained reflexes he
developed as a result of chronic parafunctions
§ physical therapy
• Posture training
• Electrotherapy
• Ultrasound
• Anesthetic block/ trigger point injections
• Acupuncture
• Laser
• Mobilization
§ pharmacologic management – Pharmacotherapy
• Analgesics (opiate or non opiate): Be careful with the pts that
addicted to analgesics
• NSAIDs: Not prescribed to pts with Crohns disease, Ulcerative
colitis, Behcet’s disease
• Corticosteroids: Given with Ca and vit D. because they have a
cumulative effect on the skeletal str and they can potentially
cause osteoporosis
• Benzodiazepines
• M relaxants
• Antidepressants: Not prescribed by dentists
o Irreversible
§ dental therapies (O equilibration) – Surgery
• occlusal therapy= last option, open bite cases usually
• orthodontic therapy
• orthognathic surgery= it is beneficial when the pt has a type of
O that contributes to TMD manifestation
• surgical approaches that involve the TMJ
o indications: disk ankylosis, large osteophytes,
hyperplasia of the coronoid process
o large osteophytes that limit the movement of the
condyle (this can happen in TMJ arthritis) or any
condition that hardens the ligaments
o M. ossificans
o Coronoid process hyperplasia
L10: Rheumatologic conditions that can affect the SS
- RA, JA, PA => Systemic arthritides= All of them belong to the group of systemic
arthritides and all of the m are considered inflammatory arthritides
o OA is NOT an autoimmune disease
- Systemic Arthritides
o Joint Inflammation
o Arthralgia
o Structural changes = General/ Systemic therapy is needed and the approach
is given by a rheumatologic
o There are also other autoimmune disorders that can affect the TMJ, such as
scleroderma, Sjogren’s syndrome, lupus erythematosus
o ALL the conditions that are presented in this lecture are autoimmune
diseases that are under a rheumatologists’s supervision and usually a dentist
plays an assisting role in the diagnosis and the monitoring of the pt
o There are hundreds of rheumatoid conditions but HERE there are the MOST
common conditions
o Clinical signs and symptoms of an ongoing chronic TMJ inflammation are
variable between pts and within the pt over time
o Signs and symptoms
§ Pain (arthralgia)
§ Swelling/ exudate
§ Tissue degradation
§ Growing disturbance
§ Resorption of the condylar str associated with malocclusion (such as
progressive open bite)
o It is NOT necessary for a patient to have all of these symptoms to receive a
diagnosis or at least to be referred to a rheumatologist!!!
o Diagnostic approach
§ Imaging: MRI (TMJ) + CBCT (TMJ). Also the same exams needed for
the joints that appear to be affected
§ Lab criteria: Elevated levels of IL-1β, IL-1Ra, IL-6, TNF, serotonin or
glutamate + Reduced levels of IL-1sRII or TMFsRII in the synovial fluid
§ If a pt receives a score of at lest 6/10 then he is diagnosed with RA.
For those that have symptoms and their score is below 6/10 they are
reassessed at a later time
§ It is not necessary to be found positive at rheumatoid factor to
receive the RA diagnosis when there are other criteria fulfilled
- OA: degenerative disease, morning stiffness lasting less then 30mins, cartilage loss,
heberden’s nodes, asymmetrical
- RA: autoimmune disease, morning stiffness lasting more than 30mins, inflamed
synovium, extra- articular involvement
o Clinical signs and symptoms for TMJ RA
§ Sensitivity or pain at palpation of the TMJ
§ Sensitivity or pain at palpated M
§ Pain at functional movements
§ Limitation of functional movments (at opening and laterotrusions)
§ Crepitus
 § TMJ stiffness
§ Increase in temperature
§ Swelling
§ Anterior open bite (at severe TMJ RA)
o Criteria for TMJ RA diagnosis
§ Bilateral attack of other TMjs
§ Sensititivity at palpation of the TMJ area (periauricular area)
§ Crepitus
§ Subchondral erosion of the osseous structures revelaed from
radiographs
§ Swelling at the acute phase
§ Temperature variations
• At the acute phase -> increase
• At chronic RA -> normal
§ Anterior open bite
§ Acute phase -> arthrocentesis reveal increased number of neutrophils
or monocytes [In chronic RA -> arthrocenetesis reveals increased
number of lymphocytes and plasma cells ]
§ If there are 4 criteria fulfilled -> diagnosis of TMJ RA
o Radiographs of affected joints by RA
o Anterior open bite, why? Because there is interruption of
the activity of the lateral pterygoid M when there is severe
attack of the condyle
§ There is limited ability for contraction of the
masseter, the temporalis, and the medial pterygoid
M, that normally elevate or protrude the mandible
o How do we handle occlusal interference? The O interferences that appear in
the anterior open bite, occur as a result of a severe inflammation of the TMJs.
This is the only case that we may consider the O equilibration, but ONLY
when the pt is in remission
§ We always ask for dental lab for guidance to estimate the amount of
enamel and dentine that needs to be filled. Always ask for ortho
assessment
o Management - The systemic disease has to be ctrl with prescriped med
§ For the TMJ approach is
§ At the acute phase: NSAIDs and analgesics, intra- articular
administration of corticosteroids if there is not response to the
previous meds. For the pts that cannot take NSAIDs they are given per
os corticosteroids. Methotrexade daily for management and in severe
cases monoclinic antibodies that are anti-TNF
§ At the chronic phase: the inflammation is mild or in remission splint,
physiotherapy, kinesiotherapy, restore dentition and occlusion
- Juveline idiopathic arthritis
o JA = describe arthritis, or inflammation of the joints, in children
o Most common symptoms = joint swelling, pain and stiffness that don’t go
away
o JA = usually autoimmune disorder. In an autoimmune disorder, the immune
system attacks some of the body’s own healthy cells and tissues
o To diagnose JA, a doctor may perform a physical exam, ask about family
health history and order lab or blood tests and x-rays
o JA can make it hard to take part in social and after school activities, and it can
make schoolwork more difficult. But, all family members can help the child
both physically and emotionally
o Exercise is key to reducing the symptoms of arthritis and maintaining range of
motion of the joints
o Inflammation inside of the eye and growth problems may also occur with JA
o 7 types
§ Systemic JIA: affects the whole body. Symptoms include high fevers,
the child may feel very ill, appear pale or develop a rash. The spleen
and lymph nodes might become enlarged
§ Oligoarthritis: affects 4 or fewer joints, often the knee or ankle.
Symptoms include pain, stiffness or swelling in the joints
§ Polyarticular negative: symptoms include swelling or pain in five or
more joints. The small joints of the hands are affected as well as the
weight – bearing joints like the knees, or ankle, feet and neck
§ Polyarticular positive: this type of JIA behaves the most like adult RA
and kids who have it have a rheumatoid factor (RF) or anti- cyclic
citrullinated peptide in their blood
§ Psoriatic negative: kids with this also have the psoriasis rash (a scaly
red rash that can start behind the ears, on the eyelids, elbows, knees
or scalp) themselves or a close relative with psoriasis
§ Enthesitis related: this type of arthritis often affects the legs and
spine. Kids also might have inflammation at the entheses – areas
where tendons join bones
§ Undifferentiated: arthritis that doesn’t fit into any of the above
categories or fits into more than one of the categories
o This is any type of arthritis that affects everyone that is younger than 18y.o.
The most common type is Juveline RA(=juveline polyarticular positive
arthritis).
o The medical management approach is the same BUT THE DOSE IS ADAPTED.
o Methotrexate and anti-TNF Biological factors
o When TMJs are affected we cannot use splints long term, but only for several
weeks during a relapse. Regular change of splints is expected because the
facial structures are growing.
o Physiotherapy is important at relapse
to relieve the pain.
o Kinesiotherapy is used at remission to
maintain the neuromuscular
coordination.
o Medication used during relapse either
for large/small joints or TMJ: NSAIDs,
analgesics, corticosteroids per os only
if needed.
 o Careful considerations of orthodontic treatment is needed=>slow
adjustments, mild forces, it is better to avoid orthognathic surgery
o UNKNOWN CAUSE
- Psoriatic Arthritis (PA) Immune system causes inflammation in your joint
o Classification of (CASPAR)
§ This method uses a points system to scale your symptoms. At least 3
points indicates psoriatic arthritis
§ Skin psoriasis
• You have it now = 2 points
• You had it = 1 pt
• You have a family history = 1pt
§ Nail lesions (piting, pulling away from the nail bed) = 1pt
§ Dactylitis (swollen, sausage- like fingers or toes – can be present or
past) = 1pt
§ Negative rheumatoid factor = you don’t test +ve for this blood protein
that signals RA = 1pt
§ Juxta- articular (near a joint) bone formation that shows up on x-ray
and isn’t bone spurs = 1pt
o Tests to diagnose PA
o Blood tests
§ These tests can help conform PA and rule out other conditions, like RA
§ Erythrocyte sedimentation rate (sed rate or ESR): Gives a rough idea
of how much inflammation is in your body, which could be caused by
psoriatic arthritis. But higher levels can come from other autoimmune
diseases, an infection, a tumor, liver disease, or pregnancy, too.
§ Rheumatoid factor (RF) and anti-CCP antibody: These tests can rule
out rheumatoid arthritis. People with that condition may have higher
levels of these in their blood.
§ HLA-B27: More than half of people who have psoriatic arthritis with
spine inflammation will have this genetic marker. You can get tested
to find out if you do.
§ Iron tests: People with psoriatic arthritis may have mild anemia , or
not enough healthy red blood cells.
o Complications of Psoriatic Arthritis
§ Having PsA can make you likely to develop other conditions over time,
some of the most common are
§ Cancer. People with PSA may be more likely to get lymphoma and
nonmelanoma skin cancer. Your treatment plan should include
regular cancer screenings.
§ Cardiovascular disease. Psoriatic arthritis can boost your risk for
cardiovascular disease like a heart attack or stroke. Talk to your
doctor about your risk and treatments that can help.
§ Crohn's disease. People with psoriatic arthritis and Crohn's share
similar changes to their genes, called mutations. That’s why there’s a
link between psoriasis, psoriatic arthritis, and inflammatory bowel
disease like Crohn's disease or ulcerative colitis. If you have both
psoriasis and psoriatic arthritis, your odds are even higher.
 § Depression. Psoriasis and psoriatic arthritis can make you more likely
to have low self-esteem and mood disorders like depression.
Depression is even more likely If you have both psoriatic arthritis and
psoriasis. But treating the psoriasis can help with your depression.
§ Diabetes. Having psoriasis and psoriatic arthritis raises your risk of
type 2 diabetes. Having severe psoriasis boosts it even higher. Tell
your doctor if you have symptoms of type 2 diabetes, such as heavy
thirst, hunger, blurry vision, or fatigue.
§ Eye inflammation and vision problems. Inflammation in the colored
part of your eye, the iris, can cause pain that gets worse in bright
light. This can cause vision problems. You'll probably need to see an
eye doctor to treat this condition, which is known as uveitis.
§ Gout. You get this form of inflammatory arthritis when uric acid
crystals form in your joints. Though you can get uric acid from food,
doctors also think it’s a byproduct of psoriasis and psoriatic arthritis.
§ Joint damage. Arthritis mutilans, a rare but destructive condition that
sometimes happens with psoriatic arthritis, rapidly damages joints at
the ends of your fingers and toes. Severe damage can interfere with
activities of daily living such as walking or dressing.
§ Metabolic syndrome. Researchers have found a link between
psoriasis, psoriatic arthritis, and metabolic syndrome -- a cluster of
conditions that include heart disease, obesity, and high blood
pressure. Women with psoriasis and anyone with severe psoriatic
arthritis may be almost twice as likely to get it as others.
o X-Rays: These can show cartilage changes or bone and joint damage that
suggests arthritis in your spine, hands, or feet. Psoriatic arthritis usually looks
different on X-rays than rheumatoid arthritis does.
o Bone Density Scan: Because psoriatic arthritis may lead to bone loss, your
doctor may want to measure your bone strength.
§ You could be at risk for osteoporosis and fractures.
o Joint Fluid Test: A type of arthritis called gout can also cause joint pain. It
happens when uric acid builds up in your system and creates crystals in your
joint fluid. To rule it out, a doctor can use a needle to take a sample of fluid
from one of your achy joints. If uric acid crystals are present, you have gout.
o The medical management approach is
o Methotrexate and/or anti-TNF Biological factors
o When TMJs are affected we use splints long term.
o Physiotherapy is important at relapse to relieve the pain.
o Kinesiotherapy is used at remission to maintain the neuromuscular
coordination.
o Medication used during relapse either for large/small joints or TMJ: NSAIDs,
analgesics, corticosteroids
- Vasculitis - The most serious types of vasculitis involve both small and medium-sized
arteries. = Takayasu arteritis, Giant cell arteritis (temporal arteritis), Polyarteritis
nodosa, Kawasaki disease, Granulomatosis with polyangiitis, Behçet's syndrome,
Eosinophilic granulomatosis with polyangiitis, Microscopic polyangiitis.
 - Temporalis arteritis: It is an autoimmune disease of the CT that causes inflammation
at the walls of the vessels
o Clinical signs and symptoms: Low fever and persistent headache that do not
subside with analgesics, fatigue, pain at the temporal area, pain at
mastication, limitation of the function of the mandible,increased muscular
sensitivity at the masseter and the sternocleidomastoid muscles, vision
problems(diplopia, partial/general blindness)
o The palpation of the temporal area is very painful to the patient and the
examiner experiences a pulsating sensation
o Giant cell arteritis facts
§ Caused by inflammation in the arteries
§ Typically affects people older than 50
§ Causes head pain, jaw pain and vision problems
§ Closely linked with polymyalgia rheumatica
o Lab exams reveal increased ESR
o At clinical exam the temporal artery is palpated under the skin and gives a
pulsating sense
o LAB EXAMS + CLINICAL EXAM + BIOPSY OF T.A. = DIAGNOSIS OF TA
o Treatment/ management
§ Corticosteroids 60-80mg daily for about 2y
§ Sometimes in combination with azathioprine (immunosuppressant)
§ The response to the corticosteroids is immediate and impressive

L11: Orofacial pain and neuropathic pain disorders

- Pain quality descriptors and secondary symptoms associated with different
categories of pain
Pain category Quality Secondary symptoms
Musculoskeletal Dull Flushing
Aching Hyperalgesia
Pressure Allodynia
Depressing Can refer to or be
Tight referred from distant
Stiff sites
Occasionally sharp Worse with function
Neuropathic Shooting Numbness
Bright Hyperalgesia
Stimulating Paresthesia
Burning Allodynia
Itchy Dysesthesia
Electric shock like
Cutting
- Hyperalgesia: a noxious stimulus is perceived as more intense or
longer than normal
o Abnormal increased sensitivity to pain, which may be caused
by damage to nociceptors or peripheral nerves and can cause
hypersensitivity to stimulus
- Allodynia: pain from a stimulus that normally does not elicit pain
 o A condition in which pain is caused by a stimulus that does not normally elicit
pain. It is different from hyperalgesia, an exaggerated response from a
normally painful stimulus
- Dysesthesia: is the abnormal sensation to the sense of touch that maybe
experienced as burning, crawling, electric- shock, cold, wet, piercing, itching. There is
a stimulus but the experience of it is abnormal
o Is the perception of the pain when no stimulus is present
- Paresthesia: it is the abnormal sensation of ‘pins and needles’ due to temporary
pressure on a nerve or it can be a symptom of nerve damage (when there is a
sensation without a stimulus)
o a burning or prickling sensation that is usually felt in the hands, arms, legs, or
feet, but can also occur in other parts of the body. The sensation, which
happens without warning, is usually painless and described as tingling or
numbness, skin crawling, or itching. Paresthesia can be caused by disorders
affecting the central nervous system, such as stroke and transient ischemic
attacks (mini-strokes), multiple sclerosis, transverse myelitis, and
encephalitis. A tumor or vascular lesion pressed up against the brain or spinal
cord can also cause paresthesia.
o Is the abnormal perception of a sensation in the absence of any stimulus
- Pain quality descriptors and secondary symptoms associated with different
categories of pain
Pain category Quality Secondary symptoms
Neurovascular Throbbing (= I wake up in Worsened by increasing
the morning and I feel a intracranial pressure (e.g.
tabbing sensation – MRA to Valsalva, bending over,
check the BV) physical activity)
Stabbing Sensitivity to light and/ or
Pounding sound nausea vomiting
rhythmic (usually with people in
chronic migraines)
Psychogenic (occlusal Descriptive Complain patterns often do
dysesthesia in schizos- not match anatomical
imaging, cold test- do not sensory supply
proceed to endo or
extraction, perform
anesthesia – if you don’t see
success stop it there -> not
odontogenic)

- Types of pain
o Primary - Same source & same site
§ Source of pain = the location where the pain actually originated from
§ Site of pain = the location where the patient describes feeling the pain
o Secondary
§ Heterotopic
• Central pain , Projected pain , Referred pain
 § Secondary pain = an underlying condition adeq accounts for the pain
or its impact (the pain is the symptom of a disease)
§ Heterotopic pain = it is the pain that is perceived in a region that has a
nerve supply different of the source of the pain (the source is
different from the site)
§ Central pain = pain appears in the peripheral str and there are
systemic symptoms, such as nausea, numbness, balance disorders,
non justifiable excessive pain
§ Projected pain = pain that is giving painful sensation at the peripheral
distributions of the nerve that is involved initially
§ Referred pain = the painful sensations are felt not in the involved
nerve but in other branches of that nerve or entirely to a different
nerve
- The central excitory effect= a phenomenon where a certain input
in the CNS (such as deep pain), can create an excitory effect on
other non associated interneurons. There are two possible ways
for this to happen (not both of them at the same time!):
o Constant and prolonged afferent iput bombards the
interneuron -> accumulation of neurotransmitter
substance in the synapses
o Convergence
- Orofacial pain
o Do the mechanisms of the somatic pain neural pathway
apply in orofacial pain? Yes but with several differences
o Which neural fibres are involved in this pathway?
§ Aδ and C
o Trigeminal nerve
o What is ganglion? A ganglion is a n cell cluster or a group
of n cell bodies located in the autonomic nervous
system and sensory system. Ganglia house the cell
bodies of afferent nerves and efferent nerves
o Gasserian ganglion: The trigeminal ganglion (or
Gasserian ganglion, or semilunar ganglion, or
gasser’s ganglion) is a sensory ganglion of the
trigeminal nerve (CNV) that occupies a cavity
(Meckel’s cave) in the dura mater, covering the
trigeminal impression near the apex of the petrus part of the
temporal bone
o The neural pathway of orofacial pain
§ The trigeminal lemniscus, also called the
trigeminothalamic tract, is composed of the ventral
trigeminal tract, and the dorsal trigeminal tract –
nerve tracts that convey tactile pain, and temperature
impulses from the skin of the face, the mucous
membranes of the nasal and oral cavities, and the eye,
as well as proprioceptive information from the facial
and masticatory muscles.
 § The trigeminal lemniscus is composed of second order neuronal axons
in the brainstem. It carries sensory information from the trigeminal
system to the ventral posteromedial (VPM) nucleus of the thalamus.
§ The oral cavity has bilateral sensory projections, whereas other facial
structures have only contralateral sensory projections
§ The ventral trigeminal tract, ventral trigeminothalamic tract, anterior
trigeminal tract, or anterior trigeminothalamic tract is a tract
composed of second order neuronal axons. These fibers carry sensory
information about discriminative and crude touch, conscious
proprioception, pain, and temperature from the head, face, and oral
cavity. The ventral trigeminal tract connects the two major
components of the brainstem trigeminal complex – the principal, or
main sensory nucleus and the spinal trigeminal nucleus, to the ventral
posteromedial nucleus of the thalamus.
§ The ventral trigeminal tract is also called the anterior trigeminal
lemniscus
§ Structure: The first order neurons (from the trigeminal ganglion)
enter the pons and synapse in the principal (chief sensory) nucleus or
spinal trigeminal nucleus. Axons of the second order neurons cross
the midline and terminate in the ventral posteromedial nucleus of the
contralateral thalamus (as opposed to the ventral posterolateral
nucleus, as in the dorsal column medial lemniscus (DCML) system).
The third order neuron in the thalamus then connects to the sensory
cortex of the postcentral gyrus.
o Trigeminothalamic pathways
§ The ventral trigeminothalamic tract carries pain and temperature
sensations from the face and oral cavity
§ The dorsal trigeminothalamic tract carries sensations of tactile
discrimination and pressure from face and oral cavity
§ REMEMBER: The oral cavity has bilateral sensory projections, whereas
other facial str have only contralateral sensory projections
o Innervation of the head and facial area
§ Trigeminal nerve
§ Intermedius nerve
§ Glossopharyngeal nerve
§ Upper cervical roots via the occipital nerves
- Pain conditions involving the nerves
o Neuralgia = the pain of a nerve
o A type of neuropathic pain
o Episodic neuropathic pain characteristics: Paroxysmal, shooting pain,
imitating, electric shock, burning pain, triggered by a harmless stimulus
o Cause = stimulation by compression, distortion, exposure to cold or other
type of irritation, lesion in the central neural pathways
- Trigeminal neuralgia: The pain is distributed at areas that are innervated by the
branches of V nerve. Most commonly V2 and/ or V3
o Usually, it appears after an injury that involves one of the branches
(traumatic extraction)
 o An innocent stimulus can trigger it (touch, shaving, cold air)
o Quality of pain: it has the typical characteristics of a neuropathic pain-
shooting pain/ burning pain/ electric shock
o Duration: 2secs up to 2mins bust appears repeatedly
- Neuropathic pain disorders
o Trigeminal neuralgia
§ Primary (classical) trigeminal neuralgia
• Classical TrN purely paroxysmal
• Classical TrN with concomitant continuous pain
§ Secondary trigeminal neuralgia
• Trigeminal neuralgia attributed to multiple sclerosis
• Trigmenal neuralgia attributed to a space occupying lesion
o Glossopharyngeal neuralgia
- Primary trigeminal neuralgia - Previously used -> Tic Douloureux
o A disorder characterized by recurrent unilateral bried electric shock-like
pains, abrupt in onset and termination, limited to the distribution of one or
more divisions of the trigeminal nerve and triggered by innocuous stimuli. It
may develop without apparent cause or be result of another disorder.
Additionally, there may or may not be concomitant continuous pain of
moderate intensity within the affected division(s)
o Diagnostic criteria
§ Recurrent paroxysms of unilateral facial pain in the distribution(s) of
oner or more divisions of the trigeminal n, with no radiation beyond
and fulfilling criteria B and C
§ The pain has all the following characteristics
• Lasting from a fraction of a second to 2mins
• Severe intensity
• Electric shock like, shooting, stabbing or sharp in quality
§ Precipitate by innocuous stimuli within the affected trigeminal
distribution
§ Not better accounted for by another ICOP or ICHD-3 diagnosis
o In a few pts, pain may radiate to another division, but remains within the
trigeminal dermatomes
o Duration can change over time, with paroxysms becoming more prolonged. A
minority of pts will report attacks predominantly lasting for >2mins
o Pain may become more severe over time
o Some attacks may be, or appear to be spontaneous, but there must be a
history or ending of pain provoked by innocuous stimuli to meet this
criterion. Ideally, the examining clinician should attempt to confirm the
history by replicating the triggering phenomenon. However, this may not
always be possible because of the patient’s refusal, the awkward anatomical
location of the trigger and/ or other factors
o Other than the triggering phenomenon, most patients with Trigeminal
neuralgia fail to show sensory abnormalities within the trigeminal territory
unless advanced methods are used (e.g. quantitative sensory testing).
However, in some patients, clinical neurological examination may show
sensory deficits. These should prompt neuroimaging investigations to explore
 the possible cause. Diagnosis of subforms such as Classical trigeminal
neuralgia, Secondary trigeminal neuralgia or Idiopathic trigeminal neuralgia is
then possible.
o When very severe, the pain often evokes contraction of the muscles of the
face on the affected side (tic douloureux).
o Mild autonomic symptoms such as lacrimation and/or redness of the
ipsilateral eye may be present.
o Following a painful paroxysm there is usually a refractory period during which
pain cannot be triggered.
- Secondary trigeminal neuralgia Trigem neuralgia caused by an underlying disease
o Clinical exam shows sensory changes in a substantial percentage of these pts
o Diagnostic criteria
§ Recurrent paroxysms of unilateral pain fulfilling criteria for trigeminal
neuralgia, either purely paroxysmal or associated with concomitant
continuous or near continuous pain
§ An underlying disease has been demonstrated that is known to be
able to cause, and explain the neuralgia
§ Not better accounted for by another ICOP or ICHD-3 diagnosis
o MRI = best equipped to detect an underlying cause of 2ary trigeminal
neuralgia. Other investigations may include neurophysiological recording of
trigeminal reflexes and trigeminal evoked potentials, suitable for pts who
cannot undergo MRI
o Recognized causes are tumor in cerebellopontine angle, arteriovenous
malformation and multiple sclerosis
o Tumor in the cerebellopontine angle
o Facial vascular malformation - reason that cause 2ary trigeminal neuralgia
o Multiple sclerosis - White matter lesions
o … attributed to Multiple Sclerosis (MS): Trigem neuralgia caused by a MS
plaque or plaques in the pons or trigeminal root entry zone, and assoc with
other symptoms and/ or clinical or lab findings of MS
§ Diagnostic criteria
• Recurrent paroxysms of unilateral facial pain fulfilling criteria
for trigeminal neuralgia
• Both of the following
o MS has been diagnosed
o An MS plaque at the trigeminal root entry zone or in
the pons affecting the intrapontine primary afferents
has been demonstrated by MRI, or its presence is
suggested by routine electrophysiological studies
showing impairment or the trigeminal pathways
• Not better accounted for by another ICOP or ICHD-3 diagnosis
§ Trigeminal neuralgia attributed to multiple sclerosis occurs in 2–5% of
patients with MS, sometimes bilaterally. Conversely, MS is detected in
only 2–4% of cases of Trigeminal neuralgia. Symptoms of trigeminal
neuralgia are rarely a presenting feature of MS. The lesion in the pons
affects the intrapontine central terminals of the trigeminal afferents
projecting to the trigeminal brainstem nuclei. Pontine lesions
 affecting the second-order neurons of the trigeminothalamic tract
usually lead to non-paroxysmal pain and/or dysaesthesias, and should
be given the ICHD-3 diagnosis of Central neuropathic pain attributed
to multiple sclerosis.
§ Some patients with MS are found to have neurovascular compression
of the trigeminal root. It is thought that MS increases the
susceptibility of the nerve root to the effects of compression, leading
more readily to painful paroxysms.
§ Patients with [Link].1 Trigeminal neuralgia attributed to multiple
sclerosis benefit less from pharmacological and surgical interventions
than those with Classical trigeminal neuralgia.
- Glossopharyngeal neuralgia: Occurs at the distribution of the glossopharengeal
nerve, and sometimes at the auricular and pharyngeal branches of the Vagus nerves
o Quality of pain: Severe, transient, stabbing, burning
o Location of pain: ear, base of tongue, tonsillar fossa, beneath angle of jaw
o Duration: 2secs – 2mins per episode, re- occurring episodes during the day
o Prev used term -> vasoglossopharyngeal neuralgia
o A disorder characterized by unilateral brief stabbing pain, abrupt in onset and
termination, in the distributions not only of the glossopharyngeal nerve but
also of the auricular and pharyngeal branches of the vagus nerve. Pain is
experienced in the ear, base of the tongue, tonsillar fossa and/or beneath the
angle of the jaw. Commonly provoked by swallowing, talking or coughing and
may remit and relapse in the fashion of Trigeminal neuralgia.
o Diagnostic criteria
§ Recurring paroxysmal attacks of unilateral pain in the distribution of
the glossopharyngeal nerve and fulfilling criterion
§ Pain has all the following char
• Lasting from a few secs to 2mins
• Severe intensity
• Electric shock like, shooting, stabbing or sharp in quality
• Precipitated by swallowing, coughing, talking or yawning
§ Not better accounted for by another ICOP or ICHD-3 diagnosis
§ Within the posterior part of the tongue, tonsillar fossa, pharynx or
angle of the lower jaw and/ or in the ear
o Imaging may show neurovascular compression of the glossopharyngeal nerve
o The pain in Glossopharyngeal neuralgia may radiate to involve the eye, nose,
chin or shoulder. It can be severe enough for patients to lose weight. In rare
cases, attacks of pain are associated with vagal symptoms such as cough,
hoarseness or syncope and/or bradycardia.
o Clinical examination usually fails to show sensory changes in the nerve
distribution but, if mild sensory deficits are encountered, they do not
invalidate the diagnosis. Major changes or a reduced/missing gag reflex
should prompt aetiological investigations.
o Glossopharyngeal neuralgia is usually responsive, at least initially, to
pharmacotherapy (especially carbamazepine or oxcarbazepine). It has been
suggested that application of local anaesthetic to the tonsil and pharyngeal
wall can prevent attacks for a few hours.