Joint Dysfunction

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© Springer Nature Switzerland AG 2021

R. Reti, D. Findlay (eds.)Oral Board Review for Oral and Maxillofacial

2. Temporomandibular Joint Dysfunction

Rishad Shaikh1  , Damian Findlay2 and Robert Reti3

Midwest Oral Maxillofacial and Implant Surgery, St. Louis, MO, USA

Oral Facial Surgery Institute, St. Louis, MO, USA

Southwest Oral Surgery, St. Louis, MO, USA

Holmlund-Hellsing lineArthrocentesisArthrotomyTotal joint replacementAnkylosisInternal derangementMyofascial pain disorderWilkes classificationMRIKaban protocolArticular diskCostochondral graft

  • The temporomandibular joint (TMJ) is a ginglymoarthrodial joint with translational movement in the superior joint space and rotational movement in the inferior joint space (Fig. 2.1).

  • The capsular ligament or joint capsule is a functional ligament that surrounds the joint (attaching to the temporal bone and surrounds the condylar head/neck circumferentially).

  • The capsular ligament is lined by the synovium, which functions to provide nutrition and immunosurveillance and lubricates the joint.

  • The other two functional ligaments are the collateral ligaments and the temporomandibular ligaments.

  • The accessory ligaments are the sphenomandibular and the stylomandibular ligaments.

  • The articular disk is composed of fibrocartilage. It has three zones (anterior band, intermediate band, and posterior band). Posterior to the disk are the retrodiscal tissues, which are highly vascular and innervated.

  • Primary joint movement is determined by the muscles of mastication (masseter, lateral pterygoid, medial pterygoid, and temporalis) and the inframandibular accessory muscles serve to impact mandibular function secondarily.

  • The vascular supply of the TMJ is primarily from branches of the superficial temporal, maxillary, and masseteric arteries.

  • The nerve supply of the TMJ is predominantly from branches of the auriculotemporal with contributions from the masseteric and posterior deep temporal nerve.

Fig. 2.1

Temporomandibular joint anatomy. (a) Lateral view. (b) Sagittal view. (Reprinted with Permission from Kadenami and Patel [9])

Myofascial Pain Dysfunction (MPD)

Definition  – non-articular TMJ disorder that manifests itself as dull regional masticatory myalgia that worsens with function and can lead to a decreased range of motion. It can involve the muscles of mastication and any combination of the supramandibular and inframandibular muscle groups. This is the most common TMJ disorder.

  • Parafunctional habits such as bruxism, nail biting, clenching, or gum chewing.

  • Life stressors.

  • Apertognathia and/or overjet greater than 6 mm.

  • Lack of posterior dentition leading to muscle hyperactivity.

Clinical Manifestations
  • Jaw pain with tenderness of the muscles of mastication and/or supramandibular and inframandibular muscles.

  • May see wear facets of the dentition.

  • Scalloping of the tongue.

  • Morsicatio buccarum, laborium, or linguarum.

  • Patients may complain of sore teeth.

  • Decreased range of motion.

  • Buccal exostoses (Wolff’s law states that bone responds to the pressure exerted on it by an osteoblastic response).

  • Patients often will complain of pain on the side of their face as opposed to pointing to the preauricular region. Pain is usually diffuse and involves the muscles of mastication (DDx of MPD-trigeminal neuralgia, atypical facial pain, fibromyalgia).

  • NSAIDS to reduce pain and inflammation (e.g., ibuprofen 600 mg QID × 2 weeks, naproxen 500 mg BID × 2 weeks, Mobic 7.5–15 mg daily for 2 weeks)

  • Occlusal appliances

  • Soft diet

  • Muscle relaxants:

    • Cyclobenzaprine 5–10 mg daily QHS, baclofen 5–10 mg TID (Some advocate for prescribing these medications TID. There is concern for dizziness/sedation, which is why some surgeons choose to prescribe it QHS.)

  • Warm compresses

  • Occlusal equilibration

  • Trigger point injections

  • Botox intramuscular injections

  • Replacing the posterior dentition

  • Physical therapy

Degenerative Joint Disease

Definition – a chronic inflammatory arthritis within the TMJ resulting in degradation of articular cartilage with remodeling of the subchondral bone.

Non-inflammatory Degenerative Joint Disease (aka Osteoarthritis)
  • Due to an imbalance between catabolic and anabolic processes. This leads to expression of catabolic cytokines (TNF-alpha, IL-1, IL-6), initiating liberation of collagenases and proteases that result in degradation of the articular cartilage. Osteoarthritis of the TMJ can be preceded by internal derangement and trauma and can also develop in patients that have had orthognathic surgery.

Inflammatory Arthritis
  • Joint destruction due to an inflammatory arthritic process (e.g., rheumatoid arthritis (RA), juvenile rheumatoid arthritis, psoriatic arthritis, gout, pseudogout, ankylosing spondylitis, reactive arthritis).

  • Depends on the extent and the level of life disruption . May include medications, physical therapy, or steroids or disease-modifying drugs.

  • For mild cases failing conservative treatments, consider arthrocentesis and arthroscopic procedures.

  • More advanced cases may require arthroplasty or total joint replacement.

Internal Derangement of the Temporomandibular Joint

Definition – disorder of the TMJ in which the articular disk is in an abnormal position as it relates to the condyle and fossa when the teeth are in occlusion. Malposition of the disk may lead to pain, instability, decreased range of motion, and abnormal mobility of the mandible.

  • Trauma

  • Joint laxity

  • Parafunctional habits

  • Altered joint lubrication system

  • Anchored disk phenomenon (disk adhesion to articular fossa)

  • MPD

  • Look for decreased maximal incisal opening (MIO) , deviation, deflection, palpable clicks (reciprocal), and crepitus. Patients often will complain of pain in the preauricular region as opposed to pointing to the side of the face.

  • Diagnosis by MRI-T1 and T2. Disk is normally displaced in an anteromedial vector. Can see osseous changes and abnormal contours of the disk.

  • Disk displacement with reduction – patient opens the mouth with an accompanying click that is produced when the condyle passes over the posterior portion of the disk. During opening, the disk returns to its normal anatomical position in relation to the fossa and condylar head. During closing, a second click can be appreciated as the condyle passes back over the thickened posterior portion of the disk.

  • Disk displacement without reduction – patient attempts to open but the condyle cannot pass over the posterior band of the disk. May see deflection to the ipsilateral side and decreased excursion to the contralateral side. This results in limitation of opening.

  • Wilkes classification classifies the degree of internal derangement and provides guidance in relation to treatment options (Table 2.1).

Table 2.1

Wilkes classification of internal derangement

Wilkes classification [1]


Clinical findings

Radiographic findings

Surgical findings

Stage I

Painless clicking No pain or locking

Anterior disk displacement noted. Disk contour remains normal with no osseous changes

Normal disk noted and displaced anteromedially

Stage II

Occasional painful clicking with intermittent locking

Anterior disk displacement noted with reduction on opening Mild disk deformity with no osseous changes

The disk appears thickened and displaced anteromedially.

Stage III

Frequent painful clicking with severe limitation in range of motion Joint tenderness noted

Anterior disk displacement noted without reduction Moderate disk deformity with no osseous changes

The disk is deformed and displaced anteromedially Adhesions may be appreciated

Stage IV

Restricted range of motion with chronic pain and joint crepitus

Anterior disk displacement noted without reduction Marked disk deformity with osseous changes

The disk is perforated with noted osseous changes of the condylar head and the fossa

Stage V

Joint pain and crepitus

Disk is displaced Marked disk deformity with severe osseous changes

The disk is perforated with noted severe osseous changes of the condylar head and the fossa

  • Conservative treatment as previously mentioned (if appropriate).

  • Intra-articular injections with a local anesthetic/steroid mixture.

  • Those unresponsive would benefit from arthrocentesis with or without arthroscopy, arthroplasty with repositioning, or meniscectomy with or without graft/replacement, or modified condylotomy.

  • Postoperative management – physical therapy/range of motion exercises.

Disorders of Hypomobility and Hypermobility

Hypomobility can be due to intra-articular factors or extra-articular factors (pseudoankylosis).

Extra-Articular Causes
  • Muscle fibrosis secondary to radiation, myofascial pain, tumors, infection, hysteric trismus, myositis ossificans.

  • Fractures involving the condyle, zygomatic arch, or coronoid process.

True ankylosis (Fig. 2.2) – intra-articular fusion within the joint space resulting in hypomobility:

  • Can be bony, fibrous, or fibro-osseous.

  • Can be complete vs. incomplete.

  • Can be caused by trauma, infection, otitis media, rheumatoid arthritis, psoriatic arthritis, prolonged immobilization, and previous TMJ or orthognathic surgery.

  • Based on radiographic findings, two commonly accepted classifications have been adopted. Topazian based on three classes and Swahney has four classes (Table 2.2).

Fig. 2.2

Ankylotic mass extending from the medial aspect of the ramus to the mandibular fossa over a previously placed prosthetic temporomandibular joint. (Image courtesy of Dr. Damian Findlay)

Table 2.2

Sawhney and Topazian classifications of ankylosis

Classification of ankylosis [2]

Sawhney (1986)

Topazian (1984)

Type 1 – flattened condylar head with close approximation to joint space

Type 2 – flattened condyle close to glenoid fossa, bony fusion on outer aspect of articular surface. No fusion of the medial joint space

Type 3 – bony block bridging the mandibular ramus and zygomatic arch

Type 4 – wider bony block bridges the mandibular ramus and zygomatic arch, completely replacing the architecture of the joint

Stage 1 – only condyle involved

Stage 2 – extends to sigmoid notch

Stage 3 – entire condyle, sigmoid notch, and coronoid

Workup for Ankylosis
  • Clinical exam – decreased MIO , inability to appreciate translation of the condylar head.

  • Orthopantogram – can see a radiodense mass, overall bony morphology, and coronoid hypertrophy.

  • CT with contrast – defines the extent of the heterotopic bone/ankylotic mass. It also delineates the relationship of the mass to vital structures (foramen ovale, foramen spinosum, carotid canal, jugular foramen , pterygoid plexus). CT also aids in fabrication of a custom TMJ prosthesis in the setting of immediate reconstruction.

Treatment Options – requires excision of the mass with reconstruction . The goal of MIO is 35 mm and greater. In an adult, the reconstruction is more commonly achieved with a prosthetic joint, which is described later in text (other options include costochondral graft (CCG) or fibula free flap).

The Seven-Step KABAN Protocol [3]
Dr. Kaban described a protocol for the treatment of TMJ ankylosis in pediatric patients:

  • Aggressive resection of the fibrous and/or bony ankylotic mass.

  • Coronoidectomy on the affected side and measure MIO intraoperatively.

  • Coronoidectomy on the contralateral side if you cannot achieve an MIO >35 mm and/or to the point of dislocation of the unaffected TMJ.

  • Lining of the TMJ with a temporalis myofascial flap or the native disk (if salvageable).

  • Reconstruction of the ramus condyle unit with either distraction osteogenesis (DO) (activate 2–4 days) or CCG and rigid fixation (10 days of MMF (Maxillary-Mandibular Fixation). If DO is used to reconstruct the ramus condyle unit, reshape the native bone narrowed and rounded. A corticotomy is then created distally to serve as transport disk. The distraction is set at 1 mm/day. Mobilization begins the day of the operation. In patients who undergo CCG reconstruction, mobilization begins after 10 days of MMF. DO takes advantage of the fibrocartilaginous cap that forms on the advancing front of the distracted bone heading toward the fossa.

  • Early mobilization of the jaw.

  • Aggressive physiotherapy.

Treatment Options for Fibrous Ankylosis
  • Can be treated more conservatively .

    • Lysis of adhesions and fibrosis.

    • Diskectomy.

Postoperative Management
  • Aggressive physical therapy is paramount in the treatment.

  • Frequent follow-up.

  • Consider radiation therapy (20 Gray in 10 fractions) to prevent recurrence and consider when using autogenous grafting, as the risk of recurrence is higher.

Costochondral Graft
  • The CCG is commonly used in the growing child. It offers many advantages including ease of adaptation and remodeling, low morbidity at the harvest site, low rate of infections, and reduced relative cost. It does, however, increase operating time. In adults 12–17 cm of rib can be harvested and 7–10 cm in children within the borders of the lateral edge of the latissimus dorsi and costochondral junction.

  • Ribs 4–7 may be harvested as they have a direct cartilaginous connection to the sternum. Rib 6 is the most commonly harvested as the incision falls in the inframammary crease creating a better cosmetic outcome (fusion of the rectus and pectoralis major forms an avascular plane.) It is common practice to harvest the right rib, as it is least likely to be confused with cardiogenic pain. Many advocate the rib contralateral to the side of the defect to allow appropriate curvature of the harvested rib.

Rib Harvest Technique [4]
  • A sharp incision is made in the inframammary crease (5 cm long).

  • Dissection is carried through the subcutaneous tissue, fascia, and the plane between the pectoralis major and rectus abdominis.

  • Two fingers are used to straddle the fifth and sixth intercostal space to prevent slipping of instruments. A sharp incision is cut through the periosteum down to the outer cortex of the rib.

  • A molt periosteal now can be used to dissect in a subperiosteal plane around the rib. Some surgeons used the Doyen rib stripper, but its usage is known to be associated with parietal pleural tears.

  • A sharp blade is used to make the cartilaginous incision. In children it is important to harvest no more than 3 cm (no less than 1 cm) to avoid overgrowth of the rib and to prevent separation of the cartilaginous cap.

  • The rib is pulled laterally and a protected rib cutter is now used to section the length of desired rib.

  • Check for pleural tears by filling the cavity with normal saline and have the anesthesiologist perform a Valsalva maneuver to check for bubble formation.

  • The periosteal sleeve is now closed with 3-0 polyglactin (this may promote de novo regeneration of the missing rib in the child patient).

  • The fascia between the rectus and pectoralis major is closed with a 3-0 resorbable suture, followed by subcutaneous tissue and finally skin.

  • Post-operatively a chest X-ray is ordered to rule out a missed pneumothorax or hemothorax. The patient may return to normal activity post-op day 7, but any strenuous activity is withheld for 6 weeks.


  • Cartilaginous Cap Has Separated from Harvested Rib – this is a highly debated question and the opinion of the authorities appears to be diverse. One approach is to drill a hole through the width of the rib and tie a non-resorbable suture to secure the cap. Another approach is to simply harvest the second rib above and start fresh. The rib directly above is preserved to prevent a cosmetic defect.

  • Pneumothorax – occurs when air is trapped between the visceral and parietal pleural cavity. The condition develops when there is a one-way valve allowing air to enter and not escape. This condition can rapidly progress to respiratory insufficiency and cardiovascular collapse. Clinically the patients will have labored (tachypneic) breathing, chest pain, tachycardia, hyper-resonance of chest wall on the affected side with diminished breath sounds. Late findings include cyanosis, distension of neck veins, tracheal deviation, and a decreased level of consciousness. Radiographically can appreciate tracheal deviation, loss of pleural lines, and loss of vascular markings (Fig. 2.3). Treatment firstly is 100% oxygen therapy to reduce the alveolar concentration of nitrogen, effectively increasing the difference in concentration of oxygen between tissue capillary and pneumothorax space, leading to rapid absorption by the surrounding vasculature. A pneumothorax 10% or less in size can be left to reabsorb and serial chest X-rays are indicated. If it does not resolve in 1 week, a tube thoracostomy is required. Estimation is provided by using a crude method by using a correlation that a 2.5-cm margin of gas peripheral to the collapsing lung corresponds to a pneumothorax of about 30%. Complete collapse of the lung is a 100% pneumothorax. If immediate pressure release is required, needle decompression can be done by placing an IV catheter at the second intercostal space along the mid-clavicular line and listen for rush of air. This procedure will normally buy time for tube thoracostomy. Tube thoracostomy requires a 2–3 cm incision that is marked at the fifth intercostal space just above the top of the sixth rib. Local anesthetic is infiltrated in the skin and tissues. A proximal end of a thoracotomy tub is clamped and advanced over the sixth rib, avoiding the neurovascular bundle on the inferior border of the fifth rib. The tube is placed on water-sealed suction drainage.

  • Pleural Tear – air bubbles may be appreciated during the Valsalva maneuver indicative of a pleural tear. A suction catheter is placed into the wound and a purse string suture through the tear. The suction catheter is removed under suction while tightening the purse string simultaneously.

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Jul 23, 2021 | Posted by in Oral and Maxillofacial Surgery | Comments Off on Joint Dysfunction
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