preprosthetic surgery and facial pain syndromes

lectures given 9/22/2026

jaw resorption after tooth loss

highly dynamic- osteoclasts break down the body’s bones including jaw bones to release needed minerals like calcium into bone

once the teeth are no longer present, the body thinks the calcium is no longer needed which then causes the bone resorption processes to occur

a section of the jaw bone that holds the teeth in the mouth (alveolar bone), will no longer receive stimuli causes bone resorption

what are the effects on jaws following tooth loss?

irregular alveolar ridge

undercuts

scarring

mucosal and muscular attachments

what are the effects of edentulism?

typical overclosed apperance

neurosensory disturbances

encroachment of muscle tissues leading to instability

prolonged effects culminates in pathological fracture

what are the general resorptive changes in an edentulous ridge?

the ridge is wide enough at its crest to accommodate the recently extracted teeth

the ridge becomes thin and pointed

the pointed ridge flattens to the level of the basal bone

the flattened ridge becomes concave as the basal bone resorbs

cawood and howell class I

dentate

cawood and howell class II

immediately post-extraction

cawood and howell class III

well rounded ridge form, with adequate height but inadequate width of the alveolar process

cawood and howell class IV

knife edge form with adequate height but inadequate width of the alveolar process

cawood and howell class V

flat ridge form with inadequate height and width

cawood and howell class VI

depressed ridge form with evident basal bone loss

what are the objectives of preprosthetic surgery?

provide a stable base through either augmentation or maintenance of the alveolar ridge at the time of surgery or alveolar ridge reconstruction after surgery

remove hard and/or soft tissue protuberances, such as frenum, tori, or hyperplastic tissue that may interfere with either insertion, retention, or stability

establish or maintain a sufficient vestibular depth to allow for denture flange for stability and retention

ridge correction procedures

hard tissue correction- alveoplasty, alveolectomy, tori/torus reduction, reduction of genial tubercles/mylohyoid ridge/maxillary tuberosity

soft tissue correction- frenectomy/frenotomy, excision of excess tissue

ridge extension procedures

vestibuloplasty

pt eval and treatment planning for preprosth surgery

no prep surgical protection should be undertaken without a clear understanding of the desired design

esthetic and functional goals of pt must be assessed

medical & surgical history, medications, allergies, psychological assessment

information on success or failure with previous prosthetic appliances may be helpful

intra oral exam

visual inspection- ridge contour, undercuts, muscle attachment, soft tissue health

palpation- denture bearing areas might reveal sharp bony areas

radiographic examination

needed to rule out bony pathology

if it is decided to leave retained roots, it should be notified to the pt

simple alveoloplasty associated with removal of a single tooth

elimiates buccal irregularities and undercut areas by removing labiocortical bone

intraseptal alveolplasty (dean technique)

removal of intraseptal bone and the repositioning of the labial cortical bone, rather than removal of excessive or irregular areas of the labial cortext

best used in an area where the ridge is of relatively regular contour and adequate height but presents an undercut to the depth of the labial vestibule because of the configuration of the alveolar ridge

can be accomplished at the time of tooth removal or in the early initial postoperative healing period

the labial prominence of the alveolar ridge can be reduced without significantly reducing the heigh of the ridge in this area

periosteal attachment to the underlying bone can also be maintained thereby reducing postoperative bone resorption and remodeling

the muscle attachments to the area of the alveolar ridge can be left undisturbed in this type of procedure

the main disadvantage of this technique is the decreased in ridge thickness

maxillary tuberosity reduction (hard tissue)

horizontal or vertical excess of the maxillary tuberosity area may be a result of excess bone, an increase in the thickness of soft tissue overlying the bone, or both

preoperative radiograph or selective probing with a local anesthetic needle is often useful to determined the extent to which bone and soft tissue contribute to this excess and to locate the floor of the maxillary sinus

recontouring of the maxillary tuberosity area may be necessary to remove bony ridge irregularities or to create adequate interarch space, which allows proper construction of prosthetics appliances in in the posterior areas

maxillary tuberosity reduction (soft tissue)

primary objective- provide adequate interarch space for proper denture construction in the posterior area, firm mucosal base of consistent thickness over the alveolar ridge denture bearing area

buccal exostosis and excessive undercuts

excessive bony protuberances and resulting undercut areas are more common in the maxilla than the mandibular

although extremely large areas of bony exostoses generally require removal, small undercut areas are often best treated by filling with autogenous or allogeneic bone material

tori removal (maxillary/palatal)

tori may have multiple shapes and configurations, ranging from a single smooth elevation to a multiloculated pedunculated bony mass

tori present few problems when the maxillary dentition is present and only occassionally interfere with speech or become ulceration from frequent trauma to the palate

occasionally tori have to be removed for coverage in the prosthesis design

what are risks of tori removal?

suture breakdown

flap necrosis

hematoma formation

palatal perforation

fracture

recurrence??

removal of soft tissue excess

before the excision of this tissue, a determination must be made whether the underlying bone should be augmented with a graft

if a bony deficiency is the primary cause of soft tissue excess, then augmentation of the underlying bone is the treatment of choice

if adequate alveolar height remains after reduction of the hypermobile soft tissue, then excision may be indicated

palatal extensions, hypermobile tissues, inflammatory hyperplasia, frenum

inflammatory hyperplasia

also called epulis fissurata or denture fibrosis

generalized hyperplastic enlargement of mucosa and fibrous tissue in the alveolar ridge and vestibular area, which most often results from ill fitting dentures

nonsurgical treatment with a denture adjustment in combination with a soft liner is frequently sufficient for reduction or elimination of this tissue initially

treatment for inflammatory hyperplasia

when the area to be excised is minimally enlarged, electrosurgical or laser techniques provide good results for tissue excision

if the tissue mass is extensive, large areas of excision using electrosurgical techniques may result in excessive vestibular scarring

simple excision and re-approximation of the remaining tissue is preferred

surgical splint or denture lined with soft tissue conditioner is inserted and worn continuously for the first 5 to 7 days, with removal only for oral saline rinses

secondary epithelialization usually takes place, and denture impressions can be made within 4 weeks

laser excision of large epulis allows complete removal without excessive scarring or bleeding

a soft relined denture can provide for additional postoperative comfort from a procedure that initially creates minimal pain

labial frenectomy

level of frenal attachments may vary from the height of the vestibule to the crest of the alveolar ridge and even to the incisal papilla in the anterior maxilla

movement of the soft tissue adjacent to the frenum may create discomfort and ulceration and may interfere with the peripheral seal and dislodge the denture

surgical technique- simple excision technique, Z plasty technique, localized vestibuloplasty with secondary epithelialization, laser assisted frenectomy

immediate dentures

offers immediate psychological and esthetic benefits to patients

functions to splint the surgical site, which results in the reduction of postoperative bleeding and edema and improved tissue adaptation to the alveolar ridge

vertical dimension can be most easily reproduced with an immediate denture technique

disadvantages include the need for frequent alteration of the dentures postoperatively and the construction of new dentures after initial healing has taken place

advanced preprosthetic surgical procedures

transpositional flap vestibuloplasty (lip switch)

vestibule and floor of mouth extension procedures

submucosal vestibuloplasty

maxillary vestibuloplasty with tissue grafting

segmental alveolar surgery in the partially edentulous pt

pain

an unpleasent sensory and emotional experience associated with or described in terms of actual or potential tissue damage

acute pain

pain that is usually temporary and results from something specific, such as a surgery, an injury, or an infection

persistent (chronic or constant) pain

a painful experience that continues for a prolonged period of time that may or may not be associated with a recognizable disease process; usually characterized as pain lasting 3 mo or longer or beyond the time of healing

breakthrough pain

pain that increases above the level of pain addressed by the ongoing analgesics; this will include incident pain and end-of-dose failure

incident-related pain

pain triggered by specific movements or activities

referred pain

pain perceived at a location other than the site of the painful stimulus; is the result of innervations of organs by afferent pain fibers which follow similar paths as the sympathetic nervous system

refractory pain

pain that is resistant to ordinary treatment

nociceptive pain (musculoskeletal/somatic pain or visceral pain)

pain caused by tissue injury in the joints, bones, muscles, and various internal organs

the pts nervous system is functioning normally, picks up the injury and transmits the information to the brain

includes- pain of the muscles, joints, connective tissues, and bones, pain of the body’s internal organs

neuropathic pain

pain initiated or caused by a primary lesion or dysfunction in the nervous system

allodynia

a non-painful stimulus felt as painful in spite of normal appearing tissues

transduction

activation of nociceptive (a delta and C fibers) in response to tissue injury

transmission

a delta fibers convey fast, sharp (first) pain

c fibers convey slow, burning (second) pain

modulation

central and peripheral mechanisms alter pain perception, influenced by emotional, cultural, and past pain experiences

what are key characteristics of trigeminal neuralgia?

unilateral, severe facial pain

paroxysmal attacks- 30 sec to 2 min

electric, shock like intensity, or stabbing

maximum intensity at onset (10/10 on numeric rating scale)

what are triggers of trigeminal neuralgia?

innoculus stimuli

like cold air, chewing, talking, brushing teeth

trigger zones often located in the affected trigeminal nerve branch (most common V2-V3)

refractory period of trigeminal neuralgia?

following an attack, a short pain-free window may occur before pain can be triggered again

what is the distribution of trigeminal neuralgia?

V1- 4%

V2- 35%

V3- 30%

V1 and V2- 10%

V2 and V3- 20%

classical trigeminal neuralgia

caused by neurovascular compression

secondary trigeminal neuralgia

caused by an underlying disease

idiopathic trigeminal neuralgia

no identifiable cause

what is the epidemiology of trigeminal neuralgia?

4-5/100,000

female predominance

M:F = 1:2 or 2:3

mean age is 40-50 yr

what is the pathophysiology of trigeminal neuralgia?

nerve injury → central and peripheral demyelination → ectopic action potentials in the sensory nerve root → paroxysmal, lancinating attacks

trigeminal neuralgia tldr

no obvious clinical or radiographic source of pain

can be triggered by innocuous stimuli but can occur spontaneously

pain is episodic and recurs- does not remain the same

lasts 30 sec to 2 min

paroxysmal, sharp, shooting, electric like shocks

local anesthesia stops the attack

refractory period is present

pressure or thermal stimuli does not affect pain

dental procedures do not help

pulpal toothache tldr

clinical and/or radiographic findings usually present

not triggered by innocuous stimuli but can occur spontaneously

pain does not remain the same- may worsen or resolve

can last several minutes

sharp, pulsating, throbbing, or dull aching

local anesthesia stops the pain

no refractory period

pressure or thermal stimuli may worsen the pain

dental procedures stop the pain

neurosurgical treatment options for trigeminal neuralgia

microvascular decompression surgery- aims to decompress trigem nerve at REZ

gamma knife radiosurgery- targets the trigem nerve distal to the REZ

persistent idiopathic facial pain (PIFP)

constant pain- pt experience continuous pain in the face or teeth throughout the day

no nerve damage- this pain occurs with no identifiable neurological defects

unique pain cycle- sleep is typically undisturbed, and many pts report a brief, pain-free period (usually less than 30min) upon waking before the pain return

most intense pain is typically found in the cheeks and upper jaw

pain intensity changes throughout the day, moderate to severe

the pain can spread to other areas such as the lower jaw, back of head, ear, shoulder, or arm

no autonomic symptoms- unlike some other conditions, pain is not accompanied by autonomic symptoms such as tearing, nasal congestion, or swelling

distinctive characteristics of persistent idiopathic facial pain (PIFP)

no neuralgic attacks- does not include sudden, sharp, or brief attacks of pain

lack of sensory deficit- not associated with sensory negative symptoms like numbness or reduced sensation, however some pts describe a feeling of swelling in the affected area

connected PDAP bc it is a specific type

how should you manage persistent idiopathic facial pain (PIFP)

avoid unnecessary surgery

invasive procedures can cause centralization of the pain, lead to chronicity of the symptom, or spread to other facial regions

persistent idiopathic facial pain (PIFP) pharamcotherapy

antidepressant- amitriptyline, duloxetine

anticonvulsant- gabapentin, pregabalin

combination therapy- antidepressants, anticonvulsants

behavioral therapy in persistent idiopathic facial pain (PIFP) management

vital component

integrates into a comprehensive treatment plan for chronic facial pain

helps pts develop effective coping strategies for daily pain management

promote a realistic understanding of their condition and treatment expectations

diagnosis of trigeminal neuralgia

based on clincal presentation and characteristics of the pain

diagnosis of persistent idiopathic facial pain (PIFP)

a diagnosis of exclusion, made in the absence of any other pathology

trigeminal autonomic cephaligia’s (TAC’s)

the pain is severe and located in the area supplied by the trigeminal nerve

lacrimation, rhinorrhea, miosis

common origin is trigeminovascular symptom, trigeminoparasympathetic reflex, or circadian brain centers

shared characteristics between TAC subtypes can make diagnosis challenging

trigeminal autonomic cephaligia’s (TAC’s) subtypes

cluster headache, paroxysmal hemicrania, SUNCT/SUNA, hemicrania continua

cluster headache

longer attacks, dramatic autonomic symptoms, and restlessness/pacing behavior

strictly unilateral

orbital, supraorbital, or temporal location

attacks last 15-180 min

1-8 attacks per day

prominent autonomic symptoms

restlessness during attacks

no response to indomethacin

verapamil, lithium are preventative treatment

oxygen and triptans are acute treatment

20-40 yrs typical onset age

males>females

imaging to exclude secondary causes

paroxysmal hemicrania

short attacks, high frequency, complete response to indomethacin

strictly unilateral

orbital, supraorbital, or temporal location

attacks last 2-30 min

5-40 attacks per day

prominent autonomic symptoms

no restlessness during attacks

complete response to indomethacin

indomethacin (dramatic effect) preventative treatment

acute treatment often not required due to short attacks

30-40 yrs typical onset age

females>males

imaging to confirm PH

SUNCT/SUNA

very short, very frequent, severe attacks with prominent eye redness and tearing

strictly unilateral

orbital or temporal location

attacks last 5-240 second

3-200 attacks per day

very prominent (esp conjunctival injection and tearing) autonomic symptoms

no restlessness during attacks

no response to indomethacin

lamotrigine, topiramate, gabapentin are preventative treatment

lidocaine nasal spray, IV lidocaine are acute treatment

40-70 yrs typical onset age

males=females

imaging is mandatory (rule out posterior fossa lesions)

hemicrania continua

continuous pain with superimposed exacerbations, 100% responsive to indomethacin

strictly unilateral

orbital, frontal, or temporal location

continuous attacks (baseline) with severe exacerbations

continuous (daily, all day) attacks

mild to moderate autonomic symptoms

no restlessness during attacks

complete response to indomethacin

indomethacin (dramatic effect) preventative treatment

NSAIDs, but indomethacin is mainstay of acute treatment

30-40 yrs typical onset age

females>males

imaging to exclude structural lesions

specific treatment response for trigeminal autonomic cephaligia’s (TAC’s)

unique medication responses help differentiate subtypes- indomethacin responsiveness in PH and HC

imaging is essential- all pts should undergo MRI to rule out secondary causes or structural brain pathology

how can you differentiate SUNCT and TN?

SUNCT has 1.5:1 male to female ratio, V1 site of pain, lasts 5-240 seconds, autonomic features are prominent, refractory period is absent

TN has 1:2 male to female ratio, V2/3 site of pain, lasts <5 sec-2min, sparse to none autonomic features, refractory period is present

painful post traumatic trigeminal neuropathy (PPTTN)

type of chronic pain that develops after an injury to the branch of trigeminal nerve

causes: extraction, RCT, orthognathic surgery, dental implants, facial trauma

onset is after the traumatic event such as trauma, surgery, RCT, wisdom teeth extraction

unilateral, usually stays in the dermatome of the affected nerve, bilateral pain can occur in more extensive injuries

moderate to severity intensity (5-8 VAS), burning/shooting

triggering mechanism is usually absent- severe allodynia, positive tinel sign (pain on the percussion over the nerve)

continuous, present most of the days, intermittent, paroxysmal

positive signs: dysesthesia, hyperalgesia

negative signs: numbness

accompany signs- feeling of swelling, foreign body, hot or cold, local redness or flushing

neurosensory testing- quantitive and dynamic, mapping of injured area, CBCT injury from dental implant

pt usually woman, 45-50 yr, undergone multiple treatment modalities

associated with substantial psychosocial burden, depression, pain catastrophizing, reduced quality of life

long term follow up- approx half of 2/3 pt reported improvement

key diagnostic criteria for painful post traumatic trigeminal neuropathy (PPTTN)

traumatic event- pain must follow an identifiable injury to the trigem nerve

neurological signs- signs of nerve dysfunction (hyperalgesia, allodynia, hypoesthesia)

timing- develops within 3 to 6 mo of the injury

most common location is premolar and molar areas

progression- the pain is initially unilateral but can later spread due to central sensitization, sometimes crossing the midline or involving the face

pain characteristics of painful post traumatic trigeminal neuropathy (PPTTN)

frequency- continuous or nearly continuous, occuring almost every day with no pain free periods

dull, aching pain, but may also feel burning or throbbing, occasional bouts of sharp, spontaneous pain

varies from mild to severe, but it is not as excruciating as the pain of typical TN

some pts report a sensation of swelling in the painful area, even when there is no physical swelling

treatment approach for painful post traumatic trigeminal neuropathy (PPTTN)

early intervention- crucial for a better prognosis, as the pain becomes harder to manage the longer it persists

a mutlidisciplinary approach that addresses psychological comorbidities is often the most effective

medication is the primary treatment, a combination of topical and systemic medications may be used to reduced the required dose of systemic drugs and minimize side effects

systemic medications for painful post traumatic trigeminal neuropathy (PPTTN)

tricyclic antidepressants- often first line, work by inhibiting the reuptake of serotonin and norepinephrine and block sodium channels, amitriptyline, nortriptyline

gabapentinoids- anticonvulasant medications often prescribed for continuous neuropathic pain, gabapentin, pregabalin

serotonin norepinephrine reuptake inhibitors- particularly useful when depression is also present, more effective for neuropathic pain than SSRI bc they block the reuptake of both NE and 5-HT, duloxetine

topical medications for painful post traumatic trigeminal neuropathy (PPTTN)

capsaicin- topical agent reduces pain by depleting substance P, a neurotransmitter that transmits pain signals, it can be applied as an ointment and is often combined with a local anesthetic to reduce the initial burning sensation

compounded gels- many other agents like lidocaine, ketamine, gabapentin, or pregabalin can be compounded into a gel to facilitate absorption through the skin

compounded gels- ketocam: ketoprofen 5% + cyclobenzaprine 2% + amitriptyline 3%, neurogel: carbamazepine 5% + amirtriptyline 2% + lidocaine 5%

what should you do if trauma is observed during a surgical procedure?

topical application of dexamethasone directly to the affected area is indicated, followed by a 6 day regimen of oral dexamethasone

in the case of damage to the IAN following implant placement…

time is of the essence

if imaging reveals contact btwn the implant and the nerve, the implant should be immediately moved away from the IAN by unscrewing or completely removing it within 36 hrs

a course of steroid therapy should be started, and any accompanying pain should be controlled with a TCA or a gabapentinoid to preven central sensitization from occurring

unfortunately when an implant has been in place for several months, removal can be difficult and the prognosis for recovery is poor- removing the implant after osseointegration through trephination is more likely to cause the pain to increase

other facial pain syndromes

burning mouth syndrome

eagle syndrome

numb chin syndrome

temporomandibular joint disorders

myofascial pain syndrome

giant cell arteritis

neurovascular facial pain