CRP of 135 mg/L in Canine Space Infection

What the Value Means

Clinical Significance in Context

1. Confirms Active Bacterial Infection

• Active odontogenic bacterial infection (typically mixed aerobic-anaerobic flora, often streptococcal + staphylococcal + anaerobes)
• The body is mounting a full acute-phase response via IL-6 - driven hepatic CRP synthesis

2. Severity Classification

3. Canine Space is a "Low-Severity" Space - But 135 mg/L is Disproportionately High

• Infection may be spreading beyond the canine space (e.g., toward the buccal space or infraorbital region)
• Possible incipient cavernous sinus thrombosis - the major feared complication of canine space infection, as the canine space has direct communication pathways to cavernous sinus via the angular/ophthalmic veins
• Underlying comorbidity (diabetes, immunocompromise) amplifying the inflammatory response
• Delayed presentation with established abscess formation

4. CRP as a Treatment Monitoring Tool

• Day 0: Elevated (e.g., 135 mg/L)
• Day 2: Should fall by ~50% (to ~60-70 mg/L)
• Day 5: Should approach near-normal (~5-15 mg/L)

Clinical Actions Indicated by CRP 135 mg/L

1. Imaging - CT with contrast of the face/neck to delineate abscess extent and rule out spread to buccal, infraorbital, or intracranial spaces
2. Incision & Drainage - Canine space is accessed via an intraoral incision above the upper lip in the canine fossa region
3. IV antibiotics - Amoxicillin-clavulanate or clindamycin; escalate to piperacillin-tazobactam if spreading or diabetic
4. Serial CRP monitoring - Repeat at 48 hours to confirm treatment response
5. Watch for cavernous sinus signs - Periorbital edema, chemosis, proptosis, ophthalmoplegia, high fever

Summary

Mesiodistal Fracture of Tooth in RCT-Treated Teeth

Definition and Classification

1. Craze line - enamel only, no symptoms
2. Fractured cusp - extends into dentin
3. Cracked tooth - incomplete, not through-and-through
4. Split tooth - complete, tooth halved into two segments
5. Vertical root fracture - begins in root, extends coronally (this is what occurs in RCT teeth)

Why RCT-Treated Teeth Are Especially Vulnerable

1. Dentin Dehydration and Embrittlement

• Loss of pulp eliminates hydraulic buffering and nutritional supply to odontoblasts
• Collagen cross-linking in root dentin changes after devitalization
• Dehydration increases Young's modulus (stiffness) - the tooth becomes brittle and less able to flex under load
• (Sedgley & Messer, 1992: endodontically treated teeth are NOT weaker in ultimate strength but show more brittle fracture behavior)

2. Loss of Tooth Structure

• Access cavity preparation removes the protective roof of the pulp chamber, especially the triangular ridges
• Over-instrumentation widens canals, thinning the dentinal walls
• The mesiodistal dimension of roots is inherently narrower than the buccolingual, making them susceptible when further dentine is removed
• Post space preparation dramatically concentrates stress at mid-root

3. Iatrogenic Factors During RCT

• Lateral condensation of gutta-percha - the most commonly implicated cause; hydraulic wedging forces directed laterally split roots mesiodistally
• Excessive obturation pressure - particularly with solid core systems
• Oversized spreaders/pluggers - tip diameter too large for the apical canal creates wedge stress
• Overzealous step-back or flaring - thinning of canal walls

4. Anatomical Predisposition

• Mesial roots of mandibular molars (narrow mesiodistal width with developmental depressions)
• Buccal roots of maxillary premolars (bifurcated, narrow mesiodistally)
• Mandibular premolars and maxillary lateral incisors are also at higher risk

5. Post-RCT Restoration Factors

• Unprotected RCT teeth (no crown) are at very high risk
• Poorly fitting posts or posts with excessive taper concentrate stress at critical zones
• Parafunctional habits (bruxism) on RCT teeth without cuspal coverage are a major precipitating factor

Clinical Features

Diagnosis

Radiographic Signs

• Lateral radiolucency along the root surface (not just periapical)
• "Halo" appearance - diffuse bone loss surrounding the entire root
• Angular bone loss at the crestal or mid-root level
• Fracture line itself is often not visible on 2D X-ray, especially in early stages

Note: Standard periapical radiographs primarily image the mesiodistal plane, so a mesiodistal fracture may be invisible on PA X-rays - the fracture line is parallel to the beam.

CBCT (Gold Standard)

• CBCT is the most reliable diagnostic tool for VRF, especially mesiodistal ones
• Shows the fracture line directly in axial cross-sections
• Accuracy is affected by metallic posts (scatter artifact) - metal artifact reduction (MAR) filters improve sensitivity
• A 2024 systematic review (PMC12303641) confirmed CBCT superiority over 2D imaging for VRF detection

Clinical Probing Test

• A narrow, isolated periodontal pocket (often 6-10 mm deep) on one surface only, with normal probing elsewhere = classic VRF sign
• Use a fine explorer or transillumination light to detect coronal crack extension

Staining

• Methylene blue dye applied after flap reflection can highlight the fracture line at surgery

Iowa Staging Index (Cracked Teeth / VRF Prognosis)

Management

Single-Rooted Teeth

• Prognosis is almost always hopeless - extraction is the standard treatment
• Attempted repairs (bonding with resin, MTA, biodentine) have been reported but long-term outcomes are poor and unpredictable

Multi-Rooted Teeth (Molars/Premolars)

Prevention (Most Important)

1. Crown all RCT posterior teeth - especially premolars and molars; cuspal coverage is mandatory
2. Avoid lateral condensation in curved or narrow canals; use warm vertical or single cone techniques
3. Use spreaders/pluggers appropriate to canal size - never force oversized instruments
4. Minimize access cavity extension - conservative endodontic access (ninja access, guided endodontics)
5. Avoid large posts in narrow mesiodistal roots (mesial roots of lower molars, buccal roots of upper premolars)
6. Nightguard for bruxers with multiple RCT teeth

Summary

Vertical Root Fracture (VRF) - Complete Clinical Review

Definition

Classification of Tooth Fractures (Context)

Incidence

• VRF accounts for ~2-5% of all tooth fractures
• Among endodontically treated teeth, incidence ranges from 4% to 32%
• 80% of VRFs are detected within 2 years of symptom onset
• Most common in: mandibular molars (mesial root), maxillary premolars (buccal root), mandibular premolars

Etiology and Predisposing Factors

A. Iatrogenic (Most Common in RCT Teeth)

B. Patient and Tooth Factors

Clinical Features

Key Clinical Signs (See et al., 2019 - most associated signs):

Note: The isolated, narrow probing defect with normal probing elsewhere is the single most important clinical clue.

Radiographic Features

Radiographic Signs to Look For:

CBCT - Gold Standard

• Provides 3D axial cross-sections that visualize the fracture line directly
• Significantly superior to periapical radiography for VRF detection
• A 2023 systematic review and meta-analysis (de Lima et al., Clin Oral Investig, PMID 36700991) confirmed that CBCT acquisition parameters significantly affect diagnostic accuracy
• Limitations: metallic posts cause scatter artifacts that obscure the fracture - use metal artifact reduction (MAR) filters
• Small field of view (FOV) + high resolution + thin slices = best protocol

Diagnosis Protocol

1. Identify susceptible teeth - RCT teeth with posts, narrow roots, posterior teeth in bruxers
2. History - When was RCT done? Any previous symptoms? Repeated treatment?
3. Clinical exam - Percussion test (vertical + lateral), palpation, periodontal probing (all surfaces, note isolated pockets)
4. Sinus tract tracing - Insert GP cone into sinus tract before X-ray to trace its origin
5. Radiographs - PA in 2+ angulations; look for halo/lateral bone loss
6. CBCT - If clinical suspicion is high but 2D inconclusive
7. Transillumination - Fiber optic light to detect coronal crack extension
8. Staining tests - Methylene blue dye after flap reflection highlights the fracture line
9. Exploratory surgery - Flap raised to directly visualize the root surface; definitive diagnosis

Differential Diagnosis

• Failed endodontic treatment (periapical pathology without lateral bone loss)
• Localized periodontitis (multiple surfaces involved, plaque-related)
• Endo-perio lesion (probing all around, not just one narrow defect)
• Cemental tear (a separate entity; can also cause bone loss; distinguished by CBCT or surgery)
• Root perforation (usually identifiable by location and history)
• External root resorption

Iowa Staging Index (Prognosis of Cracked Teeth / Early VRF)

Management

Single-Rooted Teeth

• Prognosis is hopeless in most cases
• Extraction is the standard treatment
• Implant placement after adequate healing is the preferred replacement option
• Experimental options (resin bonding, MTA, biodentine, intentional replantation) have been reported but lack long-term predictability

Multi-Rooted Teeth

Prevention

Summary

Left Atrial Appendage (LAA) - Complete Clinical Overview

Anatomy

• Located near the free wall of the left ventricle, within the pericardium
• Long, tubular, hooked structure with pectinate (crenellated) muscles inside
• Has a narrow junction (ostium) with the left atrium - unlike the right atrial appendage which is broad and triangular
• The ostium can be: oval (69%), foot-like (10%), triangular (8%), teardrop (8%), round (6%)
• Anatomical components: ostium → neck → body → tip

LAA Morphology (4 Types) - Stroke Risk Significance

Normal Physiology of the LAA

1. Natriuretic peptide secretion - releases Atrial Natriuretic Peptide (ANP) and BNP in response to increased atrial pressure/volume, regulating fluid balance and blood pressure
2. Pressure relief valve - its compliance accommodates sudden rises in left atrial pressure (e.g., during exercise or tachycardia)
3. Reservoir function - acts as a buffer during systole when the mitral valve is closed

Note: After LAA occlusion/closure, ANP levels can drop, which has implications for fluid balance post-procedure.

The LAA and Thromboembolism

Why the LAA is Prone to Thrombus in AF:

TEE (Transoesophageal Echocardiography) Findings in LAA Thrombus:

• Spontaneous echo contrast (SEC) = "smoke" appearance - reflects sluggish flow; precursor to thrombus
• LAA thrombus = echogenic mass within the LAA
• Reduced LAA emptying velocity (< 20 cm/s) = major predictor of thrombus risk
• TEE is the gold standard before cardioversion and before LAAO procedures

CHA₂DS₂-VASc Score - Stroke Risk Assessment in AF

• Score 0 (men) / 1 (women): anticoagulation not recommended
• Score ≥ 2 (men) / ≥ 3 (women): anticoagulation recommended
• Higher scores → consider LAAO if anticoagulation not tolerated

Stroke Prevention Strategies Targeting the LAA

1. Anticoagulation (First-line)

2. LAA Occlusion (LAAO) - for Anticoagulation-Ineligible Patients

A. Percutaneous/Transcatheter LAAO

B. Surgical LAA Occlusion/Amputation (Concomitant Cardiac Surgery)

• Performed during CABG, valve surgery, or Maze procedure
• Methods: amputation, stapling, epicardial clip (AtriClip, Penditure)
• LAAOS III Trial (2021): LAA occlusion during cardiac surgery in AF patients with CHA₂DS₂-VASc ≥ 2 significantly reduced ischemic stroke/systemic embolism vs. standard care over ~4 years - benefit was additive to anticoagulation
• Per Goldman-Cecil: "epicardial closure of the LAA can significantly reduce the risk of ischemic stroke or systemic embolism compared with anticoagulation alone"
• A 2024 meta-analysis confirmed reduced stroke at early AND long-term follow-up with concomitant surgical LAAO (benefit limited to patients with preoperative AF)

LAA and Catheter Ablation for AF

• LAA isolation (electrical) can be added to PVI in resistant AF cases
• Risk: LAA isolation may impair LAA mechanical function → increases thrombus risk → permanent LAA occlusion may be needed if electrical isolation is performed

Summary Table

IMAGE 1 - OMFS Clinical Note (03/03/22)

Chief Complaint (C/C)

Past Medical History (PMH)

• NKH = No Known History (of allergies/other illness)
• H/O surgery for heart - specifically:
  • DVR = Double Valve Replacement (mitral + aortic, or similar)
  • TV Repair = Tricuspid Valve Repair
  • Done 8 years back
• Current Medications:
  • Digoxin (heart rate control - likely for AF or heart failure)
  • Tab Warfarin 5 mg (anticoagulant - mandatory after mechanical valve replacement)
  • Tab Furosemide + Amiloride (loop diuretic + potassium-sparing diuretic - for fluid management/heart failure)
  • Tab Myoxin 0.125 mg (Digoxin brand - same as above, or low-dose separate entry)
  • Tab Frusi (Furosemide) 20 mg

On Examination (O/E)

• Decayed: Tooth 65 | Tooth 68 with pit (↓RS = root surface/radicular surface involvement)
• Missing, Restored, Mobile: Charted but specific teeth not fully legible

Investigation

• OPG (Orthopantomogram - full dental panoramic X-ray) - already done

IMAGE 2 - Medicine OPD Consultation Note (Unit II)

Summary of Cardiac History

• S/P DVR (Status Post Double Valve Replacement) - 8 years back - done at SGNHC, Bansbari, Kathmandu
• + TV Repair (Tricuspid Valve Repair)
• + LAA Exclusion (Left Atrial Appendage Exclusion - surgically excluded at the time of cardiac surgery to prevent stroke/thromboembolism - this connects directly to your previous question about LAA!)
• Vitals: BP 110/80, HR 68 bpm

Diagnosis

• Severe MS (Mitral Stenosis)
• S'AR (Significant/Severe Aortic Regurgitation)
• S'PR (Significant Pulmonary Regurgitation)
• S'TR, S'PAR (Significant Tricuspid Regurgitation, Pulmonary AR)

Dental Findings for this Consultation

• Planned for OPG removal of tooth with:
  • Periapical abscess (tooth 6 area)
  • Apical periodontitis (tooth 6)
  • Proximal caries (teeth 5 to 7)

Coagulation Status

• PT = 24.6 (elevated, as expected on warfarin)
• INR = 2.46 (therapeutic range for mechanical valves is 2.5-3.5)

Current Medications (D/H = Drug History)

• T. Farin (Warfarin) 5 mg x 3 days / 2.5 mg x 4 days (alternating dose regimen)
• T. Amilax 1 tab OD (Amiloride-containing diuretic)
• T. Myoxin 0.125 mg OD (Digoxin) - given 6 days/week (omit on day 7)
• T. TOR 20 mg OD (Furosemide/Torasemide - crossed out, stopped)
• T. Pancare DSR 1 tab OD (Pantoprazole gastric protection)

IMAGE 3 - Cardiology Bridging Anticoagulation Protocol Letter

WHY BRIDGING IS NEEDED

PREOPERATIVE PROTOCOL

POSTOPERATIVE PROTOCOL

Continue Throughout

• T. Amilax 1 tab OD
• T. Lanoxin (Digoxin) 0.125 mg OD - 6 days/week (omit day 7)
• Pantoprazole (Pancare DSR) 1 tab OD

Dietary Instruction

Avoid liver, green leafy vegetables, and cabbage - these are high in Vitamin K which antagonizes warfarin and can unpredictably raise INR, risking valve thrombosis.

Summary of the Entire Case

• RHD with multiple severe valvular lesions
• DVR (Double Valve Replacement) + TV Repair + LAA Exclusion done 8 years ago
• Currently on warfarin (INR ~2.46, therapeutic)
• Presenting for extraction of a chronically decayed tooth (25 years!) with periapical pathology

Warfarin + Dental Extraction - Full Protocol

STEP 1: Risk Stratification (Most Important Step)

A. Thrombotic Risk (WHY is the patient on warfarin?)

B. Bleeding Risk (What procedure is planned?)

STEP 2: The Three Clinical Scenarios

SCENARIO A - LOW Thrombotic Risk + Simple Extraction

• Check INR within 24-48 hours before procedure
• Proceed if INR is ≤ 3.5 (AAOM guideline; some say ≤ 4.0 for simple extractions)
• Use local hemostatic measures after extraction:
  • Bite on pressure pack for 30-60 minutes
  • Oxidized cellulose (Surgicel) or gelatin sponge (Gelfoam) in socket
  • Suture socket closed
  • Tranexamic acid mouthwash (5% solution, 10 mL, hold 2 min, spit) - can be given every 2 hours for first day
• Avoid NSAIDs/aspirin post-op (potentiates bleeding)
• Give written instructions: when to seek help for bleeding

Harrison's 22E: "Patients undergoing tooth extraction...rarely experience uncontrolled bleeding when warfarin anticoagulation is maintained within the therapeutic range...Embolic complications and death have been reported during subtherapeutic anticoagulation."

SCENARIO B - HIGH Thrombotic Risk + Simple Extraction

Option B1 - Continue warfarin (preferred for simple extractions):

• Check INR day before or day of procedure
• If INR 2.0 - 3.5: proceed with extraction + local hemostasis (as above)
• If INR > 3.5: postpone; adjust warfarin; recheck INR in 1-2 weeks
• If INR < 2.0: the patient is under-anticoagulated - do not proceed; adjust and recheck

Option B2 - Bridging required (for extensive surgery or when INR must drop to < 1.5):

Before restarting LMWH post-op, always assess hemostasis - active socket bleeding is a contraindication to LMWH.

SCENARIO C - If INR is too high and extraction cannot be delayed

• Give oral Vitamin K 1-2.5 mg - brings INR to < 1.5 by the next morning
• Do NOT give IV Vitamin K (over-correction, warfarin resistance for weeks)
• Check INR next day and proceed if ≤ 1.5-2.0

STEP 3: Local Hemostatic Measures (Mandatory in ALL Cases)

STEP 4: Post-Extraction Instructions to Patient

1. Bite on gauze for 30-60 minutes
2. If bleeding restarts: apply fresh gauze and bite for 20 minutes; if uncontrolled - report immediately
3. No rinsing for 24 hours
4. No smoking, no hot foods/drinks for 24 hours
5. No NSAIDs (use paracetamol for pain)
6. Soft diet for 24-48 hours
7. Continue all regular medications including warfarin (unless bridging protocol says otherwise)

Quick Decision Summary

Patient on warfarin → Extraction planned
        ↓
Assess THROMBOTIC RISK
        ↓
HIGH RISK (Mech. valve, valvular AF)?
   → Check INR
   → If INR 2.0-3.5: CONTINUE, extract with local hemostasis
   → If INR >3.5: postpone, adjust
   → If extensive surgery needed: BRIDGE with LMWH

LOW RISK (non-valvular AF, low CHADS)?
   → Check INR
   → If INR ≤3.5: CONTINUE, extract with local hemostasis
   → No bridging needed
   → Can hold 1-2 days max if needed

In ALL cases: suture socket + tranexamic acid mouthwash

Normal Mouth Opening - Complete Reference

Measurement

In edentulous patients: measure between the maxillary and mandibular alveolar crests at the midline.

True MIO = Interincisal distance + Overbite (though most clinical measurements use interincisal distance alone)

Normal Values

The JCDA defines normal as 35-55 mm (average 40 mm) - equivalent to the width of 3 fingers held together.

Gender and Age Variation

• Males have larger mouth opening than females (related to mandibular length)
• Ethnic and racial variation exists - reported mean values range from 43.3 mm (Posselt) to 59 mm (Travell, men)

Grading of Restricted Mouth Opening (Trismus)

In odontogenic space infections (e.g., masseteric space, pterygomandibular space), an MIO of 30 mm - while below average - may still allow basic dental access, while < 20 mm is alarming.

In the trismus scoring system for fascial space infections (referenced in your earlier CRP case):

• Normal = 0 points
• Moderate trismus (< 2 cm / 20 mm) = 3 points
• Severe trismus (< 1 cm / 10 mm) = 4 points

Causes of Reduced Mouth Opening

Intraoral / Dental

• Pericoronitis (wisdom tooth - pterygomandibular space involvement)
• Odontogenic abscess spreading to masseteric, pterygomandibular, or infratemporal space
• Post-extraction / post-injection trismus (needle injury to medial pterygoid)
• Dry socket (alveolar osteitis)

Musculoskeletal

• TMJ disorders (internal derangement, arthritis, ankylosis)
• Masseter/pterygoid muscle spasm
• Myofascial pain dysfunction (MPD)
• Trauma - mandibular fracture, condylar fracture, zygomatic arch fracture

Systemic / Pathological

• Tetanus (classical cause - "lockjaw")
• Oral submucous fibrosis (OSMF) - due to betel nut chewing; progressive fibrosis of submucosal tissues
• Scleroderma - skin fibrosis affects perioral tissues
• Radiation fibrosis - after radiotherapy to head/neck
• Malignancy - pterygoid muscle invasion
• Parotid abscess / deep neck infection
• Meningitis, parapharyngeal abscess

Clinical Significance in OMFS / Dentistry

Quick Clinical Aide-Mémoire

Normal MIO:     35 - 55 mm   (avg 40 mm = 3 finger widths)
Trismus cutoff: < 35 mm
Mild:           25-35 mm
Moderate:       15-25 mm
Severe:         < 15 mm
Airway risk:    < 10 mm

CT Brain Findings - Acute Subdural Hematoma (SDH)

What the Scan Shows

Diagnosis: ACUTE SUBDURAL HEMATOMA (ASDH)

Why NOT Epidural? - Key Differentiating Features

Pathophysiology

• Trauma (fall, RTA) - most common
• In elderly patients (86 years, as this patient), even minor trauma or trivial falls can cause ASDH because brain atrophy increases the distance bridging veins must travel, making them more vulnerable to shear forces

CT Density by Age of SDH

Clinical Significance & Urgency

• Acute hyperdense SDH - active/recent bleed
• Midline shift present
• Ventricular compression present
• 86-year-old patient - poor physiological reserve

1. Neurosurgical emergency consultation - stat
2. Assess Glasgow Coma Scale (GCS)
3. Surgical evacuation (craniotomy or burr hole) - indicated if:
   • Hematoma thickness > 10 mm, OR
   • Midline shift > 5 mm, OR
   • GCS drop > 2 points, OR
   • ICP > 20 mmHg
4. Reverse any anticoagulation - check if on warfarin (elderly patient), aspirin, DOACs
5. Head elevation 30°, avoid hypoxia/hypotension
6. Avoid NSAIDs, administer mannitol if signs of raised ICP

Note: This is an 86-year-old patient - age is an independent predictor of poor outcome in ASDH. Mortality in acute SDH with midline shift in elderly patients is 60-90%. Surgical decision must weigh age, premorbid function, and family wishes.

Summary

This CT brain shows a ACUTE SUBDURAL HEMATOMA - left frontoparietal, crescent-shaped, hyperdense, with mass effect and midline shift to the right. Caused by bridging vein rupture (venous bleeding). Distinguished from epidural hematoma by its crescent shape and ability to cross suture lines. This is a neurosurgical emergency.

Muscles of Mastication - Intraoral and Extraoral Evaluation

Overview: The 4 Primary Muscles of Mastication

EXTRAORAL EXAMINATION

1. MASSETER

• Ask patient to clench teeth firmly
• The superficial masseter bulges prominently under the skin
• Palpate:
  • Origin: Along the inferior border of the zygomatic arch
  • Body: Pinch the muscle belly between thumb (external) and index finger
  • Insertion: At the gonial angle and inferior border of the mandible
• Then palpate again at rest (muscle relaxed)
• For the deep masseter: palpate with mouth open (muscle under tension) - origin at temporal part of zygoma

2. TEMPORALIS

• Ask patient to clench to identify muscle belly
• Palpate bilaterally and simultaneously in three zones:
  • Anterior fibers: temple area, above and in front of ear → mainly elevation
  • Middle fibers: directly over temporal fossa
  • Posterior fibers: above and behind the ear → mainly retraction
• Palpate at rest after identifying the fibers during clenching

The temporalis tendon can also be palpated intraorally at the coronoid process (see below)

3. MEDIAL PTERYGOID (Extraoral component)

• Palpate just medial to the angle of the mandible (inferior border, medial aspect) with firm inward pressure
• Ask patient to clench - the tendon tightens
• This gives a limited external assessment; intraoral access is far better

4. LATERAL PTERYGOID (Extraoral - functional test only)

• Place thumb on patient's chin
• Ask patient to protrude mandible against resistance
• If pain is produced → suggests lateral pterygoid dysfunction/spasm
• Ask: "Which side hurts?" to lateralize

INTRAORAL EXAMINATION

1. MASSETER (Deep portion - intraoral)

• Insert index finger along the buccal aspect of the lower third molar region
• Move finger posteriorly and inferiorly toward the gonial angle
• Press laterally against the deep masseter insertion at the internal surface of the mandibular angle
• Also palpate the buccinator insertion above and below the first/second molars (accessory step)

2. TEMPORALIS TENDON (Intraoral - coronoid process)

• Mouth should be OPEN (this relaxes masseter, giving access)
• Place index finger on the anterior border of the ramus
• Move finger superiorly along the antero-medial surface of the ramus
• Reach the coronoid process at the top - this is the insertion of the temporalis tendon
• Press posteriorly and superiorly
• Palpate for tenderness

3. MEDIAL PTERYGOID (Intraoral - best access)

• Ask patient to open 10-15 mm (partial opening only)
• Slide index finger posteriorly along the buccal surface past the last molar
• At the posterior border of the last molar, curve the finger medially (inward, toward tongue)
• Press medially, posteriorly, and superiorly - this presses against the medial pterygoid muscle at its insertion on the medial surface of the mandibular angle
• Ask patient if there is tenderness or pain

• Most diagnostically important intraoral palpation point
• Tenderness almost always present in condylar displacement / occlusal imbalance
• Severe tenderness + trismus in pterygomandibular space infection
• Post-injection trismus (inferior alveolar nerve block) = needle injury to medial pterygoid

4. LATERAL PTERYGOID (Intraoral)

• Ask patient to open wide (this gives maximum access)
• Use little finger or index finger
• Move finger superiorly and posteriorly past the maxillary tuberosity (behind the last upper molar)
• Then press upward, inward (medially), and backward - you are reaching toward the infratemporal fossa
• This is the most technically difficult palpation

• Tenderness = lateral pterygoid spasm (common in anterior disc displacement, TMJ disorders)
• The lateral pterygoid's attachment to the articular disc means dysfunction here → disc displacement
• Hyperactivity pulls the disc forward → anterior disc displacement with/without reduction

Summary Table - Clinical Examination

What to Document

• 0 = No pain / normal
• 1 = Mild tenderness (patient reports discomfort)
• 2 = Moderate tenderness (patient winces)
• 3 = Severe tenderness (patient pulls away / refuses further palpation)

• Induration (hardness) = fibrosis, chronic spasm, space infection
• Fasciculation = pathognomonic of active myospasm
• Crepitus / clicking during function = assess jointly with TMJ palpation