Catherine Z, Breton P, Bouletreau P Condylar resorption after orthognathic surgery: a systematic review. Rev Stomatol Chir Maxillofac Chir Orale. 2016; 117:3-10
Handelman CS, Green CS Progressive/idiopathic condylar resorption: an orthodontic perspective. Semin Orthod. 2013; 19:55-70
Chigurupati R, Mehra P Surgical management of idiopathic condylar resorption: orthognathic surgery versus temporomandibular total joint replacement. Oral Maxillofac Surg Clin North Am. 2018; 30:355-367
Gunson MJ, Arnett GW, Formby B Oral contraceptive pill use and abnormal menstrual cycles in women with severe condylar resorption: a case for low serum 17 beta-estradiol as a major factor in progressive condylar resorption. Am J Orthod Dentofacial Orthop. 2009; 136:772-779
Mercuri LG, Edibam NR A fourteen year follow up of a patient fitted total temporomandibular joint reconstruction system. J Oral Maxillofac Surg. 2007; 65:1140-1148
Sarver DM, Janyavula S, Randy Cron Q Condylar degeneration and diseases-local and systemic etiologies. Semin Orthod. 2013; 19:89-96
Gill DJ, El Maaytah M, Naini F Risk factors for post-orthognathic condylar resorption: a review. World J Orthod. 2008; 9:21-25
Kobayashi T, Izumi N, Kojima T Progressive condylar resorption after mandibular advancement. Br J Oral Maxillofac Surg. 2012; 50:176-180
Young A Idiopathic condylar resorption: the current understanding in diagnosis and treatment. J Indian Prosthodont Soc. 2017; 17:128-135
Wolford LM Idiopathic condylar resorption of the temporomandibular joint in teenage girls (cheerleaders syndrome). Proc (Bayl Univ Med Cent). 2001; 14:246-252
Kim JH, Kim YK, Kim SG Effectiveness of bone scans in the diagnosis of osteoarthritis of the temporomandibular joint. Dentomaxillofac Radiol. 2012; 41:224-229
Larheim TA, Sano T, Yotsui Y Clinical significance of changes in the bone marrow and intra-articular soft tissues of the temporomandibular joint. Semin Orthod. 2012; 18:30-43
Larheim TA, Abrahamsson AK, Kristensen M, Arvidsson LZ Temporomandibular joint diagnostics using CBCT. Dentomaxillofac Radiol. 2015; 44
Wolford LM, Gonçalves JR Condylar resorption of the temporomandibular joint: how do we treat it?. Oral Maxillofac Surg Clin North Am. 2015; 27:47-67
Bag AK, Gaddikeri S, Singhal A Imaging of the temporomandibular joint: an update. World J Radiol. 2014; 6:567-582
Van den Wyhgaert T, Strobel K, Kampen WU The EANM practice guidelines for bone scintigraphy. Eur J Nucl Med Mol Imaging. 2016; 43:1723-1738
Tanaka E, Yamano E, Inubushi T, Kuroda S Management of acquired open bite associated with temporomandibular joint osteoarthritis using miniscrew anchorage. Korean J Orthod. 2012; 42:144-154
Huang YL, Pogrel MA, Kaban LB Diagnosis and management of condylar resorption. J Oral Maxillofac Surg. 1997; 55:114-119
Wolford LM Clinical indications for simultaneous TMJ and orthognathic surgery. Cranio. 2007; 25:273-282
Sansare K, Raghav M, Mallya SM, Karjodkar F Management-related outcomes and radiographic findings of idiopathic condylar resorption: a systematic review. Int J Oral Maxillofac Surg. 2015; 44:209-216
Arnett GW Progressive Class II development: female idiopathic condylar resorption. Oral Maxillofac Surg Clin N Am. 1990; 2:699-716
Crawford JG, Stoelinga PJ, Blihdorp PA Stability after reoperation for progressive condylar resorption after orthognathic surgery: report of seven cases. J Oral Maxillofac Surg. 1994; 52:460-466
Merkx MA, Van Damme PA Condylar resorption after orthognathic surgery. Evaluation of treatment in 8 patients. J Craniomaxillofac Surg. 1994; 22:53-58
Schendel SA, Tulasne JF, Linck DW Idiopathic condylar resorption and micrognathia: the case for distraction osteogenesis. J Oral Maxillofac Surg. 2007; 65:1610-1616
Wolford LM, Cardenas L Idiopathic condylar resorption: diagnosis, treatment protocol, and outcomes. Am J Orthod Dentofacial Orthop. 1999; 116:667-677
Sidebottom AJ Guidelines for the replacement of the temporomandibular joints in the United Kingdom. Br J Oral Maxillofac Surg. 2008; 46:146-147
Mehra J, Nadershah M, Chigurupati R Is alloplastic temporomandibular joint reconstruction a viable option in the surgical management of adult patients with idiopathic condylar resorption?. J Oral Maxillofac Surg. 2016; 74:2044-2054
Condylar resorption (CR) can be categorized into functional and dysfunctional remodelling of the temporomandibular joint (TMJ). The literature describes dysfunctional remodelling of the TMJ as idiopathic condylar resorption (ICR). Idiopathic condylar resorption (ICR) is a well-documented but poorly understood pathological entity that can occur spontaneously or post-orthognathic surgery. It predominantly affects young women, with other risk factors including Class 2 malocclusion with steep mandibular plane angles. It is distinguished by a decreased condylar head volume and ramus height, progressive mandibular retrusion and an anterior open bite. Its aetiology can be categorized into surgical and non-surgical risk factors. These include hormones, systemic disease, trauma, mechanical load and surgical risk factors, such as magnitude and direction of mandibular movement, type of surgical fixation and length of post-operative maxilla-mandibular fixation. ICR is a diagnosis of exclusion, and identified by a combination of clinical, radiographic and haematological findings. Multiple treatment options have been described in the literature, including medical management, orthodontics, orthognathic surgery, TMJ surgery, TMJ and orthognathic surgery combined, and total joint prosthesis reconstruction. Further research is required to better understand the aetiology of ICR and more long-term, controlled, multicentre clinical studies are needed to evaluate the outcomes of surgical and non-surgical management of CR patients.
CPD/Clinical Relevance: Idiopathic condylar resorption has many presentations and potential causes that can greatly impact the decisions and outcomes for orthodontic/orthognathic treatment.
Article
Condylar resorption (CR) can be categorized into functional and dysfunctional remodelling of the temporomandibular joint (TMJ).1 Functional remodelling is an ongoing process involving morphological changes of the articular structures of the joint that are not associated with significant alterations in the occlusion, whereas remodelling is dysfunctional if it adversely affects the joints and the occlusion.1 The literature describes dysfunctional remodelling of the TMJ as idiopathic condylar resorption (ICR).2 ICR has also been described in the literature as condylysis, condylar atrophy, osteoarthrosis, condylar resorption, progressive condylar resorption and avascular necrosis.1,3
ICR can be progressive, resulting in alteration of the shape and volume of the mandibular condyle, but may also go into remission.4 In remission cases, excessive joint loading, for example trauma, parafunction, orthodontics and orthognathic surgery can reinitiate the resorptive process.5 It is distinguished by a decreased condylar head volume and ramus height, progressive mandibular retrusion and an anterior open bite (AOB).1,4,5 It is a well-known, but rare, occurrence most commonly seen in young females following surgery to correct an AOB, mandibular retrognathia or long anterior face height.5 It has a reported prevalence of 1 in 5000 individuals presenting for orthodontic treatment and is reported to occur as a complication in 2–5% of post-orthognathic surgery patients, with the incidence increasing to 19–31% within a subset of patients with Class 2 malocclusion with steep mandibular plane angles.6
Pathophysiology
The TMJ is covered with a layer of fibrous cartilage. During ICR, the tissue breaks down and the outer cortex of the osseous condyle begins to resorb. This can lead to narrowing and shortening of the condylar length and sclerosis of the cortical bone. Demineralization of the bone below the cortex of the articular surface bone manifests itself as an opening of the bite, and an open rotation of the mandible.5 Resorptive changes seen on the articular eminence and fossa lead it to flatten.5
The physiology behind ICR is a result of cytokine release due to stimuli such as trauma, compression or hormone imbalance. Two cytokines particularly important in the regulation of resorption are receptor activator for nuclear factor κ B ligand (RANKL) and osteoprotegrin (OPG).7 The balance between these cytokines maintains bone integrity. Osteoblasts, T cells and synoviocytes produce these cytokines in response to other hormones or cytokines and direct stress on the cells.7 RANKL promotes bone resorption via osteoclastogenesis and osteoclastic activity. OPG, on the other hand, interferes with RANKL and blocks its action, thus preserving bone. When the RANKL:OPG ratio is elevated, osteoclastic activity is promoted and when depressed, osteoclastic activity is suppressed and osteoblastic activity predominates (Figure 1). Imbalances of RANKL:OPG in the TMJs of symptomatic patients have been shown.7
Figure 1. Pathophysiology of condylar resorption.
Hormones have been shown to affect the RANKL:OPG balance, including 17 β-oestradiol. This is a potentiator of OPG release, thus protecting bone in the face of local and systemic inflammatory factors. When deficient, OPG is not promoted, allowing inflammatory factors to inhibit new bone formation or promote bone resorption.7
Other cytokines and enzymes associated with the promotion of osteoclastogenesis, and osteoclast activities and collagen breakdown in the TMJ include tumour necrosis factor-alpha (TNF-α) and matrix metalloproteinase (MMP).7
The resorptive process is usually gradual, approximately 1–1.5 mm per year, which can lead to difficulty in initial identification of the condition.6 ICR can be unilateral or bilateral, but it is most frequently seen bilaterally, indicating a potential genetic predisposition.5
Aetiology
The aetiology of ICR remains unclear; however, risk factors are largely reported in the literature for both CR and ICR. They can be classified into non-surgical and surgical factors and both are discussed because the risk factors for CR must be excluded to accurately diagnose ICR (Table 1).
Non-surgical risk factors
Surgical risk factors
Systemic
Local
Age and gender: young females
Dento-facial deformity: Class 2 malocclusion, anterior open bite, mandibular retrognathia, clockwise mandibular rotation, mandibular plane angle >40 degrees, low posterior to anterior face height, TMJ internal derangement
Direction of mandibular movement: wide mandibular advancement, counterclockwise rotation of the mandibular proximal segment
Medial or lateral condylar torqueing with rigid fixation of the mandibular segments during surgery
Non-surgical
Systemic risk factors
Age and gender
ICR is a disease of young females in their teens or early 20s, although it is also seen in males and different age groups.1,4,5 There is a male to female ratio of 1:9.5. A retrospective cohort study reported that the oral contraceptive pill and abnormal menstrual cycles are often seen in women with severe ICR.5,7 The ratio of cortical to cancellous bone in teenagers and adolescents is less compared with adults, and this may be one of the reasons for increased susceptibility to ICR in young people.6
Hormones
The higher female to male prevalence leads many to believe that a prominent systemic factor for the pathogenesis of ICR might be related to the sex hormones.7,8 Hormones mediate biochemical changes within the TMJ, causing hyperplasia of the synovial tissues around the condylar head and further exposing the condyle to resorption.4 Oestrogen receptors have been found in TMJ synovial fluid of patients presenting with ICR.4 Gunsen et al7 have made a case of low serum 17 β-oestradiol as a major risk factor for ICR by increasing intra-articular pro-inflammatory cytokines and proliferation of periarticular tissues.4,5,7 However, this is a retrospective cohort study and prospective controlled studies are needed for further evidence.7
Prolactin may also contribute to ICR and has been shown to exacerbate cartilage and bone degradation in animal models. It is likely that prolactin contributes to an accelerated ICR that has been observed in some pregnant women.1
Corticosteroids have been reported to cause joint resorption, and changes in their levels in some individuals may initiate condylar resorption and subsequent occlusal changes.1
Systemic illness
Systemic and autoimmune diseases have been linked to CR and, therefore, must be excluded in the diagnosis of ICR. These include rheumatoid arthritis (RA), juvenile arthritis, osteoarthritis, scleroderma, ankylosing spondylitis, lupus erythematosus and Sjögren's syndrome to name a few.1,8–10
RA affects the lining of the joints, causing pain and swelling that can eventually result in bone erosion and joint deformity.9
Local risk factors
Dentofacial deformity
Patients are at higher risk of developing ICR if they have an angle Class 2 malocclusion, an AOB, an open mandibular plane angle greater than 40 degrees, a clockwise mandibular rotation, slender posteriorly inclined condylar neck and a low posterior to anterior facial height ratio.4,10 In a case series, all patients who developed ICR after mandibular advancement surgery had a clockwise rotation of the mandible, mandibular retrognathism, and erosions or deformities of the condyle, or both before treatment (Figures 2–4).11
Figure 2. Panoramic radiograph showing evidence of condylar head resorption, posterior inclination of the condylar head, short ramus height and AOB.Figure 3. Lateral cephalometric radiograph showing evidence of a posterior rotation of the mandible, an increased mandibular plane angle and AOB.Figure 4. Clinical intra-oral presentation of ICR showing evidence of an AOB and increased overjet in a patient with a posterior mandibular rotation.
It has been reported that notable deterioration of ICR after orthognathic surgery occurred in patients with documented clinical and imaging evidence of pre-operative TMJ internal derangement.6
Trauma
Trauma to the TMJ is a risk factor for development of CR. Trauma is one of the most frequent causes of mandibular asymmetry in the growing child.9 Traumatic compression of the condylar head against the posterior glenoid fossa can produce an immediate loss of some portion of the cartilage cover of the condylar head, resulting in loss of nourishment and protection, and a subsequent bony condylar lysis.9 A history of trauma must be excluded for the diagnosis or ICR.
Mechanical load
A healthy TMJ, through functional remodelling, resists and adapts to excessive mechanical loads that are frequently experienced during parafunctional habits, and orthodontic procedures, such as elastic wear and appliances.5 When the TMJ is exposed to excessive mechanical loads, and its intrinsic adaptive capacity to withstand the load is exceeded, this can result in ICR. This may occur in cases of severe trauma or orthognathic surgery.1,4–6,9,11
Other
Other risk factors for the development of ICR include conditions such as reactive arthritis, avascular necrosis and infection in the TMJ.10
Surgical
Surgical risk factors include the magnitude and direction of mandibular movement, type of surgical fixation and length of post-operative maxilla–mandibular fixation.6
A case series showed surgical contributing factors for ICR were wide mandibular advancement, counterclockwise rotation of the mandibular proximal segment, inter-maxillary fixation, rigid internal fixation, bi-maxillary osteotomies and avascular necrosis of the condyle.11
Excessive pressure on the lateral or medial pole of the condyle can lead to CR and clinical relapse after orthognathic surgery. CR after orthognathic surgery was greater in susceptible patients who underwent mandibular advancement of 10 mm or greater.6 It was also shown to be greater in patients with intra-osseous wire fixation and post-operative intermaxillary fixation.6
Diagnosis
ICR is a diagnosis of exclusion, and in most cases, no clear identifiable cause is evident. Hence, the condition is referred to as idiopathic condylar resorption. When CR is suspected, haematological investigations and advanced imaging are necessary to establish a diagnosis.6
Haematological investigations
Haematological investigations are used to rule out other conditions associated with CR, such as RA or lupus. Investigating antibodies and autoimmune markers for these conditions is important for correct treatment planning in at-risk patients. These can be undertaken by a patient's general medical practitioner. Haematological investigations may include: rheumatoid factor levels; antinuclear antibodies and anti-cyclic citrullinated peptide (anti-CCP antibody). Others include erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) elevation, indicating increased inflammation and 17 β-oestradiol.1
Specific to females, investigations may include: oestrogen, vitamin D and follicle stimulating hormone (FSH) levels. Whereas in males, specific investigations include: dehydroepiandrosterone sulphate (DHEA-S), cortisol, vitamin D and the percentage of free testosterone.1
Imaging
Panoramic and lateral cephalometric radiographs can be useful as a screening tool to assess reduction in the volume and changes in shape of the condylar head and ramus height.12 They may also display skeletal and dental class 2 deformity, high mandibular and occlusal plane angles, AOB and decreased height of ramus.13 Plain radiography has some limitations, including the fact that it cannot evaluate the centre and medial side of the condyle, and that a difference in bone mineral content of at least 30–50% is required for the detection of a bone lesion.14
Cone beam computed tomography (CBCT) with 100% specificity and 80% sensitivity in diagnosing condylar resorption,15 provides valuable information regarding the bony and soft tissue components of the TMJ. These include the size, shape, quality, articular surface and relationship of the osseous components of the TMJ.6 CBCT has replaced conventional CT as an imaging technique that provides excellent osseous detail of the TMJ with reduced radiation exposure.16 CBCT, however, provides minimal information concerning the soft tissue components of the joint compared with conventional CT.16
Magnetic resonance imaging (MRI) is used to visualize the soft tissue that is in the articular disc and the peri-articular tissues, but is less useful for the assessment of osseous degenerative disease.6,17 MRIs have a sensitivity of 78% and predictive value of 54% in diagnosing condylar resorption, and are usually taken with the mouth open and closed to assess the articular disc position and reduction. MRI can also demonstrate the presence of inflammation and osseous resorption.17 Relative advantages of CT over MRI include, better bone details and 3D assessment of congenital, traumatic and post-surgical conditions.18 Serial MRI and/or CBCT can be taken at 6–12-month intervals to assess resorption activity.12
Condylar activity also can be assessed using skeletal scintigraphy (conventional nuclear medicine), which helps to determine condylar resorption activity. Bone scans can be either conventional (planar 2D) or tomographic (single photon emission computed tomography, SPECT).19 SPECT can also be combined with low-dose CT to provide fused SPECT/CT imaging providing optimal anatomical localization of abnormal bone scan activity.19 SPECT shows positive signs of resorption with an increase in osteoblast activity of approximately 10%.20 Tracers bind to hydroxyapatite at sites of osteogenesis, which is a non-specific response of bone to a range of stimuli, including injury, infection or tumour.19 SPECT has a relatively high sensitivity at 72.2%, making it advantageous for the early diagnosis of lesions. Increased tracer uptake in SPECT indicates osteoblastic activity, with decreased uptake indicating osteoclastic activity.20 Decreased uptake is less common than increased uptake, and therefore, sometimes hard to identify, giving bone scintigraphy a low diagnostic sensitivity for purely osteolytic lesions.20 Furthermore, the specificity of SPECT is relatively low at 57.7%, and the presence or absence of arthralgia or bone alterations is not significantly associated with the uptake rates observed in the bone scans.14
Routine imaging examinations, such as radiographs and CT, can only detect anatomical changes and not condylar growth activity. This is a valuable part of the diagnosis of ICR; however, it cannot differentiate between condylar activity due to ICR and other inflammatory and hyperactivity conditions.6
There are currently no clear guidelines regarding image frequency for ICR; however, the authors recommend that patients are reviewed at 6 months and repeat radiographic or CBCT imaging is considered if there is evidence of clinical progression of resorption.
Management
A perplexing aspect of treating ICR is distinguishing between active and inactive resorption. Resorption activity should be absent for a minimum of 12 months and can be measured by serial clinical monitoring, photography, study models and imaging studies.6 It is at the discretion of the clinician to evaluate whether serial images are indicated, based on their assessment or concerns about clinically evident progression.
The position of the TMJ disc is also important, with studies showing the protective effect of disc repositioning in condylar morphology following maxillo-mandibular advancement.17
Conservative
Treatment of facial deformities associated with ICR should be deferred until the condition is believed to be in remission. Conservative TMJ management principles should always be included in the treatment, while the definitive treatment plan is being formulated with the objective of decreasing loading of the TMJ and minimizing pain and dysfunction. These include the use of non-steroidal anti-inflammatories (NSAIDs), muscle relaxants and occlusal splints.1,6,17 It has been suggested that medical management is used to stabilize the biology of resorption initiated by inadvertent treatment compression of the TMJ, or systemic disease. This can be done using several medications including TNF-α inhibitors and tetracycline, which is a known MMP inhibitor, therefore reducing or inhibiting osseous resorption.1
Management, however, often requires active clinical treatment, and it is important to exclude known local and systemic factors.
Minimally invasive
Orthodontic treatment alone can be used in milder cases with minimal AOB or for at-risk patients.12 Orthodontic camouflage can be used and temporary anchorage devices (TADs) can be used to aid in AOB correction by intruding molars.21 TADs result in absolute molar intrusion, which was previously impossible with traditional orthodontic mechanics. TADs result in counterclockwise rotation of the mandible, and the reduced overbite is increased without incisal extrusion.21 This is less invasive then other methods of AOB correction, such as maxillary impaction with or without mandibular advancement. Although absolute correction may not be achievable with orthodontics and TADs alone, in high-risk patients, this is accepted as the safest option for treatment with a lower risk of disease progression. Arthrocentesis is another suggested technique; however, it does not remove the hyperplastic synovial tissues of ICR, nor reposition the articular disc into a normal functional position. This technique has been shown to be predictably unsuccessful in treatment of ICR.13
Surgical
Orthognathic surgery alone
The rationale for orthognathic surgery alone in the management of ICR is based on the belief that CR is triggered by a transient biomechanical or physiological stimulus.6 However, a category of patients exists that has a higher risk of developing ICR after orthognathic surgery. These include females with mandibular retrognathia, an increased mandibular plane angle, presence of pre-treatment condylar atrophy, and those undergoing surgical posterior condylar displacement with upward and forward rotation of the mandible with IMF.10
Inactivity of ICR at the time of surgery is important, with a stable posterior to anterior face height ratio and no change in ramus length, chin position, or overjet at two time points at least 6–12 months apart, being a good indication for orthognathic surgery.6
The severity of the dentofacial deformity must be assessed, and the surgeon must determine whether this can be corrected to achieve the desired facial changes and occlusion. The risk of ICR is 20 times more likely in cases with mandibular advancement greater than 10 mm compared with those of 5 mm.10 Mandibular surgery carries the risk of reinitiating the resorption even in stable cases.6 Advancing the mandible physically lengthens the Class III lever arms, which increases the loading on the TMJ.6 If mandibular surgery is necessary, movements of large magnitude should be avoided.6 Procedures, such as genioplasty, along with mandibular advancement or maxillary posterior impaction, can be considered rather than mandibular advancement alone.6,10 Maxillary impaction alone should be considered, if possible, for the correction of anterior open bites in at-risk patients.10
Patients with complete resorption of the condylar head and/or the posterior facial height is <35 mm are not usually good candidates for orthognathic surgery alone.6,22 Presence of TMJ dysfunction and a displaced intra-articular disc and decreased bone mineral density are risk factors that may adversely affect the outcome of orthognathic surgery in patients with ICR.23
Many studies have demonstrated less than ideal outcomes, with a high rate of relapse when orthognathic surgery alone is used for treating ICR.24–26 Revision osteotomy may be required in up to 50% of patients with ICR owing to poor aesthetics and occlusal instability after orthognathic surgery procedures.27 Therefore, cases must be selected carefully with in-depth risk-factor analysis.
Distraction osteogenesis
Distraction osteogenesis has been recommended as a treatment for major maxillofacial skeletal deformities, including ICR, because the incremental increase in bone allows the soft tissue to adapt, producing a more stable result. This technique claims to reduce the insult to the condyle compared with that which occurs with routine mandibular orthognathic surgery.28
Combined orthognathic and TMJ surgery
Wolford and Cardenas developed a method of treating ICR where the hyperplastic synovial tissue is surgically removed from the TMJ, and the articular disc is repositioned and stabilized to the condyle by using a Mitek mini-anchor placed in the posterior aspect of the condylar head, with two sutures attached, functioning as artificial ligaments.13,29 A prospective cohort study showed the importance of disc position in the treatment of ICR by evaluating three patient groups.30 Relapse following counterclockwise rotation and mandibular advancement was compared in groups with the articular disc in normal position, displaced discs repositioned with Mitek anchors and displaced discs left in place. Following an average 31-month follow-up there was a 1% relapse in the group with the articular disc repositioned with Mitek anchors, 5% relapse in the group with the articular disc in normal position and 28% for the group with the displaced discs left untreated.30
Some authors emphasize the importance of assessment of the position of the articular disc before treatment and its impact on success and longevity of treatment. However, further controlled studies are required.
TMJ reconstruction in ICR cases has traditionally been performed using costochondral grafts, and more recently, using prosthetic TMJ joint replacement. The British Association of Oral and Maxillofacial Surgeons has formulated guidelines for the replacement of the TMJ with a prerequisite being failed conservative management diagnosed with CT or MRI rather than plain radiographs alone.31 Degenerative joint disease (osteoarthritis), inflammatory joint disease (rheumatoid arthritis) and post-operative condylar loss are some of the qualifying conditions for replacement of the TMJ as per the guidelines.31
Costochondral grafts can undergo remodelling and resorption, which can lead to post-surgical occlusion changes.6 Consideration should be taken to use TMJ disc repositioning, in conjunction with TMJ reconstruction, for the treatment of ICR due to the protective quality of the articular disc on the mandibular condyle.17 Alloplastic prosthesis are now favoured by some authors because they reduce the risk of a second surgical procedure;8,32 however, these cannot be used in those who have not completed growth and long-term follow-up studies are required in this area. It is believed that there is no post-surgical remodelling, so the mandibular position remains stable and the longevity of the prosthesis is high.8,32 TMJ joint replacement can be combined with orthognathic surgery to treat ICR.6
Conclusion
Clinicians treating young patients for correction of dentofacial deformities should recognize clinical signs associated with risk of ICR. Other causative factors of dentofacial deformities must be excluded to ensure an accurate diagnosis. Patients should be appropriately educated about all treatment options, from conservative to surgical, while being informed of the risks of relapse and possible need for further treatment.
Careful case selection is of utmost importance for both conservative and surgical approaches, with the aim of treatment to ensure that condylar resorption has ceased, a stable occlusion with a functional TMJ is achieved, and that facial aesthetics are improved.
Further research is required to better understand the aetiology of ICR and more long-term, controlled, multicentre clinical studies should be developed to evaluate the outcomes of surgical and non-surgical management of CR patients.
