All posts by DentMistry

Pleomorphic adenoma

Oral Pathology
  • The commonest salivary gland tumor
  • 60 – 85% of parotid tumours
  • 45 – 50% of minor gland tumors

Most common intra-oral site: Palate (other – parotid)

Incidence: 5th – 6th decades, F = 60% cases

Clinical: A slow growing, painless, rubbery swelling with intact overlying skin

NB: CA in PSA, 3% of tumors

Histology:

  • A mixture of epithelial & mesenchymal components (myxoid, chondroid & mucoid areas, with architectural diversity)
  • Pseudoencapsulated with both intra- and extracapsular nodules representing growth of pseudopodia into the surrounding tissues → high recurrence rate

Diagnosis:

  • FNA
  • Core needle biopsy
  • Radio, US, CT, MRI

Management:

  • Surgical resection
  • Parotid – Superficial or total parotidectomy

Picture

Salivary gland tumors

Oral Pathology

Salivary gland tumors exhibit paradoxical behavior:

  • Malignancies – indolent
  • Benign tumors – aggressive

Incidence:

  • Parotid – 65%
  • Submandibular glands – 10%
  • Sublingual glands < 1%
  • Minor salivary glands – 25%

For the intra-oral tumors:

  • Palate – 55%
  • Upper lip – 20%

Tumorigenesis

Two theories:

1. Bicellular theory: Neoplasms arise from stem cells in excretory and intercalated ducts

  • Intercalated ducts:
    • Pleomorphic adenoma
    • Warthin’s tumor
    • Oncocytoma
    • Acinic cell
    • Adenoid cystic
  • Excretory ducts:
    • Mucoepidermoid
    • Squamous cell

2. Multicellular theory: Neoplasm develops from various differentiated cells within the salivary gland unit

  • Acinar cells: Acinic cell carcinoma
  • Intercalated duct: Pleomorphic tumor
  • Striated duct: Oncocytic tumor
  • Excretory duct:
    • Mucoepidermoid
    • Squamous cell
Salivary duct

WHO classification of salivary gland tumors:

1) Adenomas: Benign

2) Carcinomas: Malignant

  • Mucoepidermoid carcinomas
  • Acinic cell carcinomas
  • Adenoid cystic carcinomas
  • Carcinoma arising from PSA
  • Pleomorphic low grade adenocarcinoma
  • Others

Other causes of inflammation – Salivary gland disease

Oral Pathology

Granulomatous disease

1. Sarcoidosis

Uncommon chronic multisystem disease, unknown cause


Epidemiology: Adult females of African origin

Clinical:

  • Granuloma formation in:
    • Lungs lymph nodes (particularly hilar nodes)
    • Salivary glands
    • Oral sites
  • Systematic features:
    • Erythema nodosum
    • Lymphadenopathy
    • Lung involvement
  • Oral features:
    • Enlarged salivary glands
    • Xerostomia
    • Gingival hyperplasia
    • Labial swelling

NB: Heerfordt’s syndrome (salivary and lacrimal swelling, facial palsy and uveitis) is rare

Picture

2. TB

  • Primary TB of the salivary glands:
    • Uncommon, usually unilateral, parotid most common affected
    • Believed to arise from spread of a focus of infection in tonsils
  • Secondary TB – may involve the salivary glands but tends to involve the SMG

3. Cat Scratch Disease

  • Does not involve the salivary glands directly, but involves the periparotid and
    submandibular triangle lymph nodes
  • May involve SG by contiguous spread
  • Bacteria is Bartonella Henselae(G-R)

Picture

Cysts


True cysts of the parotid account for 2-5% of all parotid lesions

  1. Congenital:
  • Type 1 – Branchial arch cysts
  • Type 2 – Cysts are a duplication anomaly of the membranous and cartilaginous EAC
  1. Acquired:
  • Mucus extravasation vs. retention
  • Traumatic
  • Benign epithelial lesions
  • Association with tumors:
    • Pleomorphic adenoma
    • Adenoid Cystic Carcinoma
    • Mucoepidermoid Carcinoma
    • Warthin’s Tumor

Pneumoparotitis

  • Aka: pneumosialadenitis, wind parotitis, pneumatocele glandulae parotis
  • In the absence of gas-producing bacterial parotitis, gas in the parotid duct or gland is assumed to be due to the reflux of pressurized air from the mouth into Stenson’s duct.
  • May occur with episodes of increased intrabuccal pressure – glass blowers, trumpet players
  • Crepitations on palpation of gland
  • Swelling may resolve in minutes to hours, in some cases, days.
  • US and CT show air in the duct and gland
  • Antibiotics to prevent superimposed infection

Sialosis/Sialadenosis

Oral Pathology
  • Non inflammatory, non neoplastic swelling of salivary glands
  • Usually bilateral and painless, affecting the parotids

Etiology: Dysregulation of the autonomic innervation of the salivary glands.

  1. Drugs: Alcohol, Sympathomimetics (isoprenaline)
  2. Endocrine: Acromegaly, Diabetes mellitus, Pregnancy
  3. Metabolic: Liver cirrhosis, Anorexia nervosa/bulimia, Cystic fibrosis, Malnutrition
  4. HIV

Picture

Salivary duct obstruction

Oral Pathology

Sialolithiasis/salivary gland calculus

Etiology:

  • Xerostomic meds
  • Water hardness
  • Hypercalcemia
  • Tobacco smoking – cytotoxic effect on saliva, ↓ PMN phagocytic, ↓ salivary proteins
  • Gout – only systemic disease known to cause salivary calculi and these are composed of uric acid

Submandibular duct:

  • Inorganic deposits in the submandibular duct
  • Initiated by a nidus (which is frequently of bacterial origin) – acts as a focus for dystrophic calcification
  • The submandibular duct (wharton’s) is commonly affected due to:
  1. Its tortuous course and longer duct – which encourages stasis within the duct
  2. Higher mucous content in saliva
  3. Saliva more alkaline
  4. Higher concentration of calcium and phosphate in the saliva
  5. Tendency of the saliva to flow against gravity – leaching of inorganic residues
  • Ductal defects aggravate this condition – strictures and stenoses

Clinical:

  • Unilateral, painful salivary gland swelling + intermittent symptoms that appear on salivation
  • Acute ductal obstruction – may occur at meal time when saliva producing is at its maximum, the resultant swelling is sudden and can be painful (gustatory pain)
  • Gradually reduction of the swelling can result but it recurs repeatedly when flow is stimulated.
  • This process may continue until complete obstruction and/or infection occurs

Clinical history:

  • History of swellings / change over time
  • Trismus
  • Pain
  • Variation with meals
  • Bilateral
  • Dry mouth, dry eyes
  • Recent exposure to sick contacts (mumps)
  • Radiation history
  • Current medications

Examination:

1. Inspection:

  • Asymmetry (glands, face, neck)
  • Diffuse or focal enlargement
  • Erythema extra-orally
  • Trismus
  • Medial displacement of structures intraorally
  • Examine external auditory canal (EAC)
  • Cranial nerve testing

2. Palpation:

  • Palpate for cervical lymphadenopathy
  • Bimanual palpation of floor of mouth in a posterior to anterior direction
    o Have patient close mouth slightly & relax oral musculature to aid in detection
    o Examine for duct purulence
  • Bimanual palpation of the gland (firm or spongy/elastic)

Histology:

  • Prolonged obstruction – atrophy of the acini.
  • A sialolith is distinguished by its calcific lamellar appearance

Radiology:

  • Plain occlusal film
  • Nearly 50% of calcifications are diffuse/ radiolucent so if the obstruction cannot be
    visualized on a plain xray, a sialogram should be done

NB:

  • 80-90% of SMG calculi are radio-opaque
  • 50-80% of parotid calculi are radiolucent
  • 30% of SMG stones are multiple
  • 60% of Parotid stones are multiple

Other diagnostic approaches:

  1. CT Scan:
  2. Ultrasound: Can detect small stones (>2mm), inexpensive, non-invasive
  3. Sialography:
    • Opacification of the ducts – retrograde injection of a water-soluble dye.
    • Provides image of stones and duct morphological structure
    • Disadvantages:
      • i. Irradiation dose
      • ii. Pain with procedure
      • iii. Possibility of perforation
      • iv. Infection dye reaction
      • v. Push stone further
      • vi. Contraindicated in active infection
  4. Radionuclide studies:
    • Useful to image the parenchyma
    • T99 – artificial radioactive element that – used as a tracer in imaging studies
    • Half life of 6 hours
    • Shares the Na-K-Cl transport system on the BM of the parotid acinar cells
  5. MRI Sialography:
    • Advantage: No dye, no irradiation, no pain
    • Disadvantage: Cost, possible artifact
  6. Diagnostic sialendoscopy:
    • Allows complete exploration of the ductal system, direct visualization of duct
      pathology
    • Success rate of >95%2
    • Disadvantage:
      • Technically challenging
      • Trauma could result in stenosis
      • Perforation

Management:

  • Duct dilatation – to milk out the sialolith/ calcifications.
  • None: antibiotics and anti-inflammatories
  • Stone excision:
    • Lithotripsy
    • Interventional sialendoscopy
    • Simple removal (20% recurrence)
  • Gland excision

If patients defer treatment, they need to know:
– Stones will enlarge over time
– Seek treatment early if infection develops
– Salivary gland massage and hyper-hydration when symptoms develop

Stone composition:

  • Organic – often predominate in the center
  • Glycoproteins
    • Mucopolysaccharides
    • Bacteria
    • Cellular debris
  • Inorganic – often in the periphery
    • Calcium carbonates & calcium phosphates in the form of hydroxyapatite

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Mucoceles

Salivary gland cysts

Etiology: Pooling of saliva in tissues – secondary to trauma to a salivary gland

Classification: Pooling of saliva occurs:

  • Within the gland – Retention cysts
    • Salivary duct blocked – expansion and formation of cysts
    • Epithelial lined
    • Adults
  • Outside the gland – Extravasation cysts
    • Trauma – saliva spills into the tissues
    • Not epithelial lined
    • Kids
    • Neck cyst – extravasation cyst

Picture

NB:

  • Cysts located on the floor of the mouth are called ranulas (Usually the
    extravasation type) Picture
  • Ranulas can be superficial or unilateral
  • Superficial ranulas: due to trauma to 1 or more excretory ducts of sublingual
    salivary gland
  • If they burrow through the mylohyoid muscle (weak muscle), they are termed
    plunging ranulas. Picture
  • The other common site is the lower lip.
  • If the upper lip is involved, consider neoplasia

Common site: Lower lip > Floor of mouth > Palate > Buccal mucosa

Histology:

  • Compressed fibrous CT
  • Surrounding pooled, eosinophilic mucin
  • Containing macrophages that have ingested mucin (mucinages)
  • If retention cyst – epithelial lining and dilated duct
  • If extravasation – no epithelial lining, remnants of ruptured salivary gland

Management: Surgical resection, excision, recurrences are common

Sialadenitis

Oral Pathology

Inflammation of salivary gland

Risk factors:

  • Systemic dehydration (salivary stasis)
  • Chronic disease and/or immunocompromise
  • Neoplasms (pressure occlusion of duct)
  • Sialectasis (salivary duct dilation) increases the risk for retrograde contamination. Is associated with cystic fibrosis and pneumoparotitis
  • Extremes of age
  • Poor oral hygiene
  • Calculi, duct stricture
  • NPO status (stimulatory effect of mastication on salivary production is lost)
  • Sialolithiasis – mechanical obstruction of the duct resulting in salivary stasis and subsequent gland infection

Pathology:

  1. Retrograde contamination of the salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity.
  2. Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection

Acute suppurative infection

More common in parotid gland

  • Etiology: the retrograde infection from the mouth
  • 20% cases are bilateral
    • Suppurative parotitis
    • Surgical parotitis
    • Post-operative parotitis
    • Surgical mumps
    • Pyogenic parotitis
  • Predilection for parotid: Parotid is primarily serous
  • Differentials for parotid gland enlargement:
    • Lymphoma
    • Actinomycoses
    • Cat-scratch disease
    • Sjogren’s syndrome
    • Wegener’s granulomatosis
    • Viral infection

NB: Calculus formation is more likely to occur in submandibular gland duct (85-90% of salivary calculi are in the SMG duct) However, the parotid gland remains the most common site of acute suppurative infection

Picture

Bacterial sialadenitis

Pathology:

  • Mucoid saliva contains lysozymes & IgA antibodies – protect against bacterial infection (therefore, parotid has ↓ bacteriostatic activity)
  • Mucins contain sialic acid – which agglutinates bacteria and prevents its adherence to host tissue
  • Specific glycoproteins in mucins bind epithelial cells competitively inhibiting bacterial attachment to these cells

Diagnosis: Purulent saliva sent for culture

a) Acute bacterial sialadenitis

  • Uncommon disorder
  • Usually involving the parotid gland as an ascending infection

Etiology:

  • Strep pyogenes
  • Staph aureus
  • Strep viridans
  • Haemophilus
  • Debilitated/ dehydrated patients
  • Sjogren syndrome
  • Immune compromised patients

Clinical:

  • Gland swelling
  • Pain, fever, malaise
  • Redness of overlying skin
  • pus discharge
  • Trismus/lockjaw
  • Cervical lymphadenopathy

Management:

  • Reverse the medical condition that may have contributed to formation
  • Discontinue anti-sialogogues
  • Warm compresses, maximize OH, give sialogogues (lemon drops)
  • External salivary gland massage if tolerated
  • Antibiotics:
    • 70% of organisms produce B-lactamase or penicillinas
    • Need B-lactamase inhibitor like Augmentin or Unasyn or 2nd gen cephalosporin
    • Can adding metronidazole or clindamycin to broaden coverage
  • Failure to respond:
    • After 48 hours the patient should respond
    • Add 3rd gen cephalosporine
    • Add aminoglycoside
    • MRSA in nursing homes and nosocomial environments – vancomycin
  • Surgery for acute parotitis:
    • Limited role for surgery
    • Discrete abscess – surgical drainage
    • Approach is anteriorly based facial flap with multiple superficial radial incisions created in the parotid fascia parallel to the facial nerve
    • Close over a drain

Complications:

  • Hematogenous spread
  • Direct extension- Abscess ruptures into external auditory canal and TMJ
  • Fascial capsule around parotid deep surface is weak – it is adjacent to the loose areolar tissues of the lateral pharyngeal wall (Achilles ‘heel of parotid). Therefore extension of abscess- in parapharyngeal space may result in:
    • Airway obstruction
    • Mediastinitis
    • Internal jugular thrombosis
    • Carotid artery erosion
  • Dysfunction of one or more branches of the facial nerve – rare
  • Thrombophlebitis – retromandibular vein or facial veins – rare

b) Chronic bacterial sialadenitis

  • Non specific inflammation
  • Associated with long term diseases of the salivary gland
  • Parotid more common

Clinical:

  • Unilateral swelling
  • Tenderness
  • Inflamed duct orifice
  • Purulent or salty discharge

Histology:

  • Duct dilatation
  • Hyperplasia of duct epithelium
  • Periductal fibrosis
  • Acinar atrophy
  • Chronic inflammatory infiltrate

Sialography:

  • Duct obstruction or stricture
  • Destruction of glandular tissue
  • Duct dilatation (sialectasia)

Management:

  • Treat predisposing factor – calculus or stricture
  • Initial mx should be conservative:
    • Sialagogues
    • Massage
    • Antibiotics for acute exacerbations.
  • Should conservative measures fail, consider removing the gland

Viral sialadenitis

Etiology:

  • Droplet spread, incubation 2 – 3 weeks
  • Mumps = acute, contagious infection mainly caused by paramyxovirus (RNA virus)
  • Others causes of acute viral parotitis: coxsackie a & b, echo virus, cytomegalovirus and adenovirus

Clinical:

  • Fever, malaise
  • Painful swelling affecting the parotids (only in 70% of patients)

Physical exam:

  • Glandular swelling (tense, firm) Parotid gland involved frequently, SMG & SLG
  • Displace ispilateral pinna
  • 75% cases involve bilateral parotids, may not begin bilaterally (within 1-5 days may
    become bilateral)….25% unilateral
  • Low grade fever

Complications:

  • Orchitis in 20% adult males (ensuing infertility is rare)
  • Oophoritis – Ovary inflammation
  • Pancreatitis
  • Meningitis OR meneigoencephalitis
  • Deafness

Diagnosis:

  • IgM antibody titres
  • ↑ Serum amylase
  • ↑ Lipase
  • Leukocytopenia, with relative lymphocytosis

Management:

  • Antipyretics
  • Analgesics
  • Adequate hydration
  • Isolate the patient 6 – 10 days after the onset of symptoms because the virus is in the saliva at this time

Prevention: MMR Vaccine: measles, rubella, mumps vaccine is administered in a single subcutaneous dose after 12 months of age. Booster at 4-6yr

Post irradiation sialadenitis

  • Common dose-related complication of radiotherapy
  • Causes fibrous replacement of damaged acini & squamous metaplasia of ducts.
  • Sialoliths = calcification within salivary duct, involves salivary gland also occur in 70 – 90% cases

Clinical:

  • Pain & sudden enlargement of gland in relation to gustatory stimuli
  • It is complicated by ascending infection & chronic sialadenitis

Histology:

  • Acinar destruction and in case of sialolithiasis
  • lamellated structure composed of CaPO4 & CaCO3

Necrotizing sialometaplasia

Etiology: Ischaemia → infarction of salivary lobules

  • Uncommon disorder, may be mistaken for malignancy
  • Iatrogenic origin, possibly a reaction to ischemia or injury

Clinical: Deep crater-like mucosal ulcer, commonly on hard palate, persist for upto 8 weeks

Histology:

  • Histologically may be mistaken for SCC
  • Lobular necrosis of salivary glands
  • Squamous metaplasia of ducts
  • Mucous extravasation
  • Inflammatory infiltrate surrounded by pseudoepitheliomatous hyperplasia

Picture

Salivary gland diseases

Oral Pathology

Developmental anomalies

  • Aplasia: Failure to form of the entire gland system or a constituent eg duct
  • Atresia: Duct blockage
  • Heterotopic tissue: Angle/ body of mandible, Stafne’s idiopathic bone cavity

Causes of salivary gland swelling

  1. Inflammation/ Sialadenitis*
    – Acute and chronic bacterial
    – Viral
    – Post irradiation
    – Necrotizing sialometaplasia
    – Sjogren’s syndrome
  2. Duct obstruction*
    – Sialolithiasis
    – Mucoceles
  3. Neoplasms
  4. Sialosis*
  5. Drugs
  6. Deposits eg amyloid.
  7. Cystic fibrosis (rare!)
  8. Other causes of inflammation:*
    – Granulomatous dx
    – Cysts
    – Pneumoparotitis

A) Sialadenitis

B) Sjogren’s syndrome

C) Salivary duct obstruction

D) Sialosis/Sialadenosis

E) Other causes of inflammation

Age changes in salivary glands

– Weight reduction
– Atrophy of secretory tissue
– Replacement with fibro-fatty tissue
– Oncocytic change (large cells, granular cytoplasm)

Salivary gland diseases

Jaw bone pathology: TMJ diseases and disorders

Oral Pathology

TMJ anatomy

  • Condyle moves anteriorly on opening
  • Condyle moves posterior on closing
Anatomy of TMJ
  • Articular surface of bones are covered by fibrocartilage
  • Joint covered by fibrous capsule – a fibrous membrane, attaches to articular eminence, articular disc and neck of mandibular condyle
TMJ capsule
  • Articular disc is a fibrous extension of the capsule
  • Articular disc splits the joint into two synovial joint cavities, each lined by synovial membrane
  • The anterior disc attaches to the joint capsule and superior head of lateral pterygoid
  • The posterior portion attaches to mandibular fossa and is referred to as the retrodiscal tissue
  • Retrodiscal tissue is vascular and highly innervated, therefore a major contributor to pain of TMJ
Articular surfaces and disc
  • Three ligaments provide stability to the joint:
    • Temporomandibular ligament
    • Sphenomandibular ligament
    • Stylomandibular ligament
Temporomandibular ligament
Sphenomandibular ligament Stylomandibular ligament
  • TMJ muscles:
    • Temporalis – Elevation, retraction and lateral deviation of mandible
    • Lateral pterygoid – Depress, protrude and lateral deviation of mandible
    • Medial pterygoid – Elevate mandible and lateral deviation to opposite side
    • Masseter – Elevate mandible
TMJ muscles

Classification of TMJ disorders

  1. Congenital disorders:
  2. Growth disorders:
  3. Infections:
  4. Trauma:
    • Extracapsular: Condylar fracture
    • Intracapsular: Dislocation, disc displacement, ankylosis
  5. Ankylosis:
    • Bony or fibrous
    • Intracapsular (true ankylosis) or extracapsular (pseudocapsular)
  6. Dislocation:
    • Unilateral
    • Bilateral
  7. Internal derangement: Meniscal pathology
  8. Degenerative disorders:
    • Rheumatoid arthritis
    • Osteoarthritis
  9. Tumors:
    • Benign
    • Malignant
  10. Myofascial pain dysfunction syndrome (MPDS)

Symptoms associated with TMJ dysfunction:

  • CLICKING: Disk displacement.
  • LOCKING: Disk deformity + Adhesion
  • DISLOCATION: Displacement of the condyle (Single/recurrent episodes of inability to close the mouth)
Classification of temporomandibular joint disease and disorders

Ankylosis

Epidemiology: Children (2-12 years), adolescents (12-17 years)

Classification:

Classification of ankylosis

Causes:

Clinical presentation:

  • Facial asymmetry (frontal view)
  • Mandibular deficiency (profile view): Birds beak
  • No or reduced TMJ motility – leading to poor oral hygiene, carious lesions, malnourished
  • Deviation of mandible to affected side in case of unilateral ankylosis
  • Malocclusion

Radiology:

  • Fusion of joint: “Mushroom” type bony union
  • Hyperplasia of coronoid process
  • Mandibular hypoplasia
  • Malocclusion

Objectives of management:

  • Restore mandibular growth
  • Restore function
  • Restore mouth opening
  • Restore esthetics
  • Prevent relapse

Management:

  • Aggressive resection
  • Ipsilateral/contralateral coronoidectomy
  • Lining of TMJ with temporalis fascia
  • Reconstruction of TMJ (costochondral graft)
  • Aggressive physiotherapy
  • Orthodontic and secondary orthognathic surgery
  • For long standing bilateral TMJ ankylosis:
    • Osteoarthrotomy: Condylectomy + bilateral coronoidectomy
    • Ramus osteotomy
    • Angle osteotomy
    • Total joint replacement: Indication:
      • Re-ankylosis
      • Failed autogenous graft/resorption of autograft
      • Failed previous alloplastic reconstruction
      • Severe inflammatory joint disease
      • Multiple previous surgeries

Complications of surgery:

  • Trauma to external auditory meatus
  • Damage to tympanic membrane
  • Hemorrhage – Maxillary artery, pterygoid plexus
  • Damage facial nerve
  • Paresthesia/anesthesia – Auriculotemporal nerve
  • Tear of dura mater – Middle cranial fossa
  • CSF leakage

Internal derangement

  • Abnormal location of the disk in relation to other components of the joint
  • A click sound on opening indicates a displaced meniscus
  • Late stages – intermittent locking of the jaw when the patient tries to open the mouth
  • Limited opening shows bilateral disease while deviation (towards affected side) shows unilateral disease
  • Causes of internal derangement are:
    • Microtrauma – parafunctional habits eg bruxism
    • Macrotrauma – coup and counter-coup injuries

Wilkes classification:

Wilkes classification of internal derangement
  • Stage 1 and 2: Disc displacement and reduction on opening
  • Stage 3 and 4: Disc displacement and no reduction, therefore no clicking sound
  • NB: A clicking joint does not lock and a locking joint does not click

Management:

Conservative aims:

  • Reduce pain and discomfort
  • Decrease inflammation in muscles and joints
  • Improve jaw function

Methods of conservative treatment:

  • Patient education
  • Medication
  • Physical therapy
  • Splints

Surgical treatment options:

  1. Arthrocentesis – joint aspiration
  2. Arthroscopy
  3. Arthrotomy + disc repair (eg. perforation)
  4. Arthrotomy + disc reposition
  5. Arthrotomy + discectomy
  6. Arthrotomy + discectomy + autologous graft
  7. Alloplastic joint replacement
  8. Condylotomy

Inflammatory changes in TMJ

A. Primary inflammatory changes:

  • JRA (Juvenile rheumatoid arthritis)
  • JPsA (Juvenile psoriatic arthritis)

B. Secondary inflammatory changes:


I) Direct extension of adjacent inflammatory change/infection:

  • Otitis media
  • Mastoiditis (direct extension, thrombophlebitis, hematogenous spread)
  • Osteomyelitis of temporal bone/ mandibular condyle

II) Hematological spread of infection (septicemia) resulting in septic arthritis:

  • Typhoid fever (or via otitis media/mastoiditis)
  • Peritonsillar abscess
  • Scarlet fever
  • Measles
  • Pneumonia
  • Meningitis
  • Bacterial endocarditis
  • Septic pharyngitis S
  • Sinusitis

Rheumatoid arthritis

A progressive destructive disease of bone – characterized by granuloma formation – starting in the joints of the hands and feet – spreading to affect weight bearing and minor joints


Etiology: Production of auto-antibody production against abnormal antigens in the joint tissues (rheumatoid factor)

Incidence: Temperate climates, middle aged female patients

Clinical:

  • Bilateral joint stiffness
  • Crepitus
  • Tenderness and swelling
  • Fever, malaise and fatigue
  • Dermal subcutaneous nodules in 25% of patients

Pathology:

  1. Genetic susceptibility: 65% – 80% of patients have HLA-DR4/1 & 75% have an RA specific motif in the DRB1-HV3 region of their T cells
  2. A primary exogenous arthritogen: EBV, retroviridae, parvoviridae, mycobacteria, borrelia and mycoplasma
  3. Autoimmune reaction mediated by cytokines

Radiology:

  • Pannus formation = proliferation of the synovial membrane
  • Condylar lipping + marginal proliferation

Histology:

  • Fibrinoid necrosis in rheumatoid nodules
  • Surrounded by epithelioid histiocytes, lymphocytes and plasma cells

Picture

Juvenile chronic arthritis

Epidemiology: 70 % patients are female

Clinical:

  • Little/no pain
  • Limitation of movement
  • Micrognathia
  • Anterior open bite

I) JRA:

  • Destruction of condylar process from articular surface
  • TMJ pain
  • Headache
  • Tenderness of joint & muscles (temporal, masseter & sternomastoid)

II) JPsA:

  • Chronic inflammatory arthritis in children under 5 years of age
  • Classical rash
  • Dactylitis (severe inflammation of the finger and toe joints – Sausage fingers)
  • Nail pitting
  • Onycholysis (painless detachment of the nail from the nail bed)
  • Family history

Picture

Gout

Articular crystal deposits (tophi) – due to acute and chronic bone disorders

Stages of gout progression:

  1. High uric aid levels – uric acid is building up in the blood and starting to form crystals around joints
  2. Acute gout – symptoms start to occur, causing a painful gout attack
  3. Intercritical gout – periods of remission between gout attacks
  4. Chronic gout – gout pain is frequent and tophi form in joints

Picture

Osteoarthritis

A disorder of movable joints – deterioration and abrasion of articular cartilage with new bone formation at the joint surface.

Subtypes:

  • Primary: Insidious age change
  • Secondary:
    • Secondary to repetitive overload of the joint
    • Underlying systemic disease eg diabetes

Clinical:

  • Heberden’s nodes (osteophytes develop in phalanges)
  • Crepitation sounds from joints
  • Restricted/normal mouth opening capacity (normal is 3 finger breadth)
  • Pain/no pain from joint area and mastication muscles

Radiology:

  • Condylar erosion
  • Eburnation
  • Subchondral sclerosis
  • Flattening of articular eminence
  • Osteophytes (bone projections)

Management:

  • Physical therapy
  • Pulsed electrical stimulation
  • Topical ointments
  • Supplements
  • Steroid injections – Corticosteroids only relieve pain but does not treat, therefore damaging the joint more
  • Hyaluronic acid injections
  • Acupuncture

Picture

TMJ pain dysfunction syndrome

AKA Myofacial pain dysfunction syndrome (MPDS)

A multifactorial syndrome of neurological, psychological and dental origins.

Etiology: Bruxism, masticatory muscle spasm, emotional status

Clinical: Laskin’s 4 signs:

  1. Unilateral pain – in front of the ear, over the joint
  2. Pain in related facial, jaw and neck muscles
  3. Associated limitation & deviation of jaw opening
  4. Clicking or popping sound in the joint

Negative characteristics:

  1. Absence of clinical, radiographic or biochemical evidence of organic changes in TMJ
  2. Lack of tenderness in TMJ area when palpated via EAM

Management:

  • Detailed examination
  • Panoramic tomography
  • Conservative approach: Occlusal splint, psychologist referral, relaxation techniques or low dose diazepam
  • Botox for masseter, temporalis and pterygoids
  • Soft diet, avoid excessive gum chewing
  • Gentle massage at TMJ area, warm and cold compresses

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