Management of Orofacial Manifestations of Juvenile Idiopathic Arthritis: Interdisciplinary Consensus-Based Recommendations.

Involvement of the temporomandibular joint (TMJ) is common in juvenile idiopathic arthritis (JIA). TMJ arthritis can lead to orofacial symptoms, orofacial dysfunction, and dentofacial deformity with negative impact on quality of life. Management involves interdisciplinary collaboration. No current recommendations exist to guide clinical management. We undertook this study to develop consensus-based interdisciplinary recommendations for management of orofacial manifestations of JIA, and to create a future research agenda related to management of TMJ arthritis in children with JIA. Recommendations were developed using online surveying of relevant stakeholders, systematic literature review, evidence-informed generation of recommendations during 2 consensus meetings, and Delphi study iterations involving external experts. The process included disciplines involved in the care of orofacial manifestations of JIA: pediatric rheumatology, radiology, orthodontics, oral and maxillofacial surgery, orofacial pain specialists, and pediatric dentistry. Recommendations were accepted if agreement was >80% during a final Delphi study. Three overarching management principles and 12 recommendations for interdisciplinary management of orofacial manifestations of JIA were outlined. The 12 recommendations pertained to diagnosis (n = 4), treatment of TMJ arthritis (active TMJ inflammation) (n = 2), treatment of TMJ dysfunction and symptoms (n = 3), treatment of arthritis-related dentofacial deformity (n = 2), and other aspects related to JIA (n = 1). Additionally, a future interdisciplinary research agenda was developed. These are the first interdisciplinary recommendations to guide clinical management of TMJ JIA. The 3 overarching principles and 12 recommendations fill an important gap in current clinical practice. They emphasize the importance of an interdisciplinary approach to diagnosis and management of orofacial manifestations of JIA.

RE: Biomechanical comparative analysis of temporomandibular joint, glenoid fossa and head of the condyle of conventional models prothesis with new PEEK design.

This is a Letter to the Editor that describes some of the biomechanical concerns with the statements made in This is a LTE that raises some biomechanical statements made in Genovesi W, Comenale IC, Genovesi Filho W, Veloso Fernandes M. Biomechanical comparative analysis of temporomandibular joint, glenoid fossa and head of the condyle of conventional models prothesis with new PEEK design. J Oral Biol Craniofac Res. 2022 Sep-Oct; 12(5):529-541.

Preoperative Arterial Coil Embolization for Temporomandibular Joint (TMJ) Surgery in Children with TMJ Ankylosis.

ABSTRACT: Temporomandibular joint (TMJ) ankylosis in children can alter facial development and affect oral hygiene and function. Surgical release of the ankylosis is the mainstay of treatment. The authors hypothesize that preoperative arterial coil embolization is safe and effective in preventing major blood loss during TMJ surgery (loss prompting blood transfusion or hemodynamic instability requiring vasoactive medication administration) in children with TMJ ankylosis. Patients < 16 years who were diagnosed with TMJ ankylosis (<15 maximal interincisal opening) and had embolization before surgery in the last 5 years were included. Out of 9 initial search results, 3 patients were excluded (age > 16). Information gathered were patient demographics, diagnostic imaging, procedural details, complications, and clinical outcomes. Six patients, mean age 11.14 years (range 7-15 years) year and a mean weight of 40.8 ± 19 kg were included. Underlying etiologies for TMJ ankylosis: Pierre Robin Syndrome (n = 2), juvenile rheumatoid arthritis (n = 1), Goldenhar's syndrome (n = 1), trauma (n = 1), and micrognathia (n = 1). Neck computed tomography angiogram before embolization demonstrated an intimate approximation between the internal maxillary artery (IMAX) and/or external carotid artery and ankylotic mass in all patients. Eight successful embolizations were performed without procedural complication. In 1 patient with angiographic evidence of surgical internal maxillary artery ligation, embolization was performed via collaterals. Surgery was performed within 48 hours of embolization. Airway access during surgery was via nasal intubation (n = 4), oral intubation (n = 3). The estimated blood loss (EBL) during surgery was 78.33 ± 47.08 ml. Three patients had subsequent TMJ surgery with a mean estimated blood loss of 73.33 ± 46.18 ml. After a mean follow-up of 17 ± 15 months, patients showed a 13.8mm mean increment of maximal interincisal opening with 95% CI (5.74-21.9), P < 0.007.

MMPs in tissues retrieved during surgery from patients with TMJ disorders relate to pain more than to radiological damage score.

Orofacial pain is among the most common chronic pain conditions and can result from temporomandibular disorders (TMDs) of the temporomandibular joint (TMJ). Matrix metalloproteinases (MMPs) drive degeneration of TMJ tissues and likely mediate pain in TMJ disorders given their role in nociception. However, few studies have assessed MMPs in the TMJ innervated tissues nor in the context of pain. This study defined the extent of MMP-1, MMP-9, and MMP-2 in TMJ tissues from patients undergoing total joint replacement (TJR) or arthroplasty discectomy for painful TMJ disorders. Protein expression was probed by Western blot in TMJ disc and capsular ligaments taken during TJR (n = 6) or discectomy (n = 3) for osteoarthritis or internal derangement in an IRB-approved study. Pro- and active MMP-1, active MMP-9, and pro- and active MMP-2 are detectable. MMP-1 and MMP-9 correlate positively to each other (Kendall's τ = 0.63; p = 0.01), strengthening the hypothesis that they are mechanistically related in regulatory cascades. Active MMP-1 and active MMP-9 correlate positively with self-reported pain scores (τ ≥ 0.51; p ≤ 0.04), suggesting their involvement in peripheral nociception. Overall, neither MMPs nor pain correlate with the functional vertical opening of the jaw. MMP-1 varies with the observed stage of degeneration during surgery (p = 0.04). Neither overall MMPs nor pain correlate with the overall magnetic resonance imaging scores, corroborating the longstanding, but confounding, clinical observation that pain and radiological evidence of joint damage are not always related. Clinical significance: These findings suggest that MMPs mediate pain in innervated soft tissues and may be targets for diagnosing disease stage and treatments in painful TMJ disorders.

Painful temporomandibular joint overloading induces structural remodeling in the pericellular matrix of that joint's chondrocytes.

Mechanical stress to the temporomandibular joint (TMJ) is an important factor in cartilage degeneration, with both clinical and preclinical studies suggesting that repeated TMJ overloading could contribute to pain, inflammation, and/or structural damage in the joint. However, the relationship between pain severity and early signs of cartilage matrix microstructural dysregulation is not understood, limiting the advancement of diagnoses and treatments for temporomandibular joint-osteoarthritis (TMJ-OA). Changes in the pericellular matrix (PCM) surrounding chondrocytes may be early indicators of OA. A rat model of TMJ pain induced by repeated jaw loading (1 h/day for 7 days) was used to compare the extent of PCM modulation for different loading magnitudes with distinct pain profiles (3.5N-persistent pain, 2N-resolving pain, or unloaded controls-no pain) and macrostructural changes previously indicated by Mankin scoring. Expression of PCM structural molecules, collagen VI and aggrecan NITEGE neo-epitope, were evaluated at Day 15 by immunohistochemistry within TMJ fibrocartilage and compared between pain conditions. Pericellular collagen VI levels increased at Day 15 in both the 2N (p = 0.003) and 3.5N (p = 0.042) conditions compared to unloaded controls. PCM width expanded to a similar extent for both loading conditions at Day 15 (2N, p < 0.001; 3.5N, p = 0.002). Neo-epitope expression increased in the 3.5N group over levels in the 2N group (p = 0.041), indicating pericellular changes that were not identified in the same groups by Mankin scoring of the pericellular region. Although remodeling occurs in both pain conditions, the presence of pericellular catabolic neo-epitopes may be involved in the macrostructural changes and behavioral sensitivity observed in persistent TMJ pain.

Increased substance P and synaptic remodeling occur in the trigeminal sensory system with sustained osteoarthritic temporomandibular joint sensitivity.

INTRODUCTION: Temporomandibular joint (TMJ) pain is among the most prevalent musculoskeletal conditions and can result from atypical joint loading. Although TMJ pain is typically self-resolving, 15% of patients develop chronic TMJ pain that is recalcitrant to therapy and may be attributed to changes in pain processing centers. Although TMJ overloading induces pain and osteoarthritis, whether neuronal modifications in the trigeminal sensory system contribute to persistent TMJ pain is unknown. OBJECTIVE: This study investigates changes in excitatory neuropeptides and synaptic transmission proteins in cases of transient and persistent TMJ sensitivity in a rat model. METHODS: Rats underwent repeated jaw loading that produces transient (2N-load) or persistent (3.5N-load) sensitivity. In both groups, immunolabeling was used to assess substance P in the spinal trigeminal nucleus caudalis (Sp5C) and glutamate transporter 1 in the ventroposteriomedial thalamus early after loading. Synaptosomal Western blots were used to measure synaptic proteins in the caudal medulla and thalamus at a later time after loading. RESULTS: Substance P increases transiently in the Sp5C early after loading that induces persistent sensitivity. However, glutamate transporter 1 is unchanged in the ventroposteriomedial thalamus. At a later time, synaptosomal Western blots show loss of the presynaptic tethering protein, synapsin, and the inhibitory scaffolding protein, gephyrin, in the thalamus with persistent, but not transient, sensitivity. No changes are identified in synapsin, phosphorylated synapsin, homer, or gephyrin in the caudal medulla. CONCLUSIONS: Substance P in the Sp5C and later loss of inhibitory synapses in the thalamus likely contribute to, or indicate, persistent TMJ pain.

Early changes in brain network topology and activation of affective pathways predict persistent pain in the rat.

Adaptations in brain communication are associated with multiple pain disorders and are hypothesized to promote the transition from acute to chronic pain. Despite known increases in brain synaptic activity, it is unknown if and how changes in pathways and networks contribute to persistent pain. A tunable rat model that induces transient or persistent temporomandibular joint pain was used to characterize brain network and subcircuit changes when sensitivity is detected in both transient and persistent pain groups and later when sensitivity is present only for the persistent pain group. Brain activity was measured by F-FDG positron emission tomography imaging and used to construct intersubject correlation networks; network connectivity distributions, diagnostics, and community structure were assessed. Activation of subcircuits was tested by structural equation modeling. Findings reveal differences in the brain networks at day 7 between the persistent and transient pain groups, a time when peripheral sensitivity is detected in both groups, but spontaneous pain occurs only in the persistent pain group. At day 7, increased (P ≤ 0.01) clustering, node strength, network segregation, and activation of prefrontal-limbic pathways are observed only in the group that develops persistent pain. Later, increased clustering and node strength are more pronounced with persistent pain, particularly within the limbic system, and decrease when pain resolves. Pretreatment with intra-articular etanercept to attenuate pain confirms that these adaptations are associated with pain onset. Results suggest that early and sustained brain changes can differentiate persistent and transient pain, implying they could be useful as prognostic biomarkers for persistent pain and in identifying therapeutic targets.

Outcomes and Survivorship of Biomet Microfixation Total Joint Replacement System: Results From an FDA Postmarket Study.

PURPOSE: In February 2011, the Food and Drug Administration issued a postmarket surveillance order to all manufacturers of temporomandibular joint (TMJ) implants in the United States. The objective of the present study was to measure implant subsequent surgical intervention (SSI) among patients who had undergone TMJ reconstruction with the Biomet TMJ replacement system (Zimmer Biomet, Warsaw, IN). MATERIALS AND METHODS: A prospective observational study was conducted by sending a questionnaire to patients who had received a Biomet TMJ replacement system from 1995 to 2010 in the United States. The questionnaire was sent annually from 2012 to 2015. The primary endpoint was the SSIs. SSIs included both device removal and reoperations. Kaplan-Meier survival analysis was used to determine the survivorship, and Cox proportional hazard regression analysis was performed to evaluate the preoperative diagnosis and SSI. RESULTS: The mean age at implantation was 46.6 ± 12.5 years, with a gender distribution of 86.1% female. Data from 499 joints in 319 subjects were collected as a part of the survey. The mean follow-up time was 8.6 ± 3.9 years (range, 2-20 years). The first SSI frequency was 11.2% (4.2% removal rate and 7.0% reoperation rate). The survivorship rate (Kaplan-Meier) was 96% at 3 years, 94% at 5 years, and 86% at 10 years. The mean interval to failure using a survival function to determine the time to SSI (Greenwood's formula) was 13.5 ± 0.193 years. The most common causes of SSI included adhesion removal (2.6%; 13 of 498), heterotopic bone/ankylosis (2.0%; 10 of 498), and infection (1.6%; 8 of 498). CONCLUSIONS: The results from the present study are consistent with the reported survivorship rates for other orthopedic devices (5-year survival for total hip or knee arthroplasty, 95.9 and 97.2%, respectively). The etiology of SSIs in the Biomet TMJ replacement system was primarily secondary to biologic failure (ie, adhesions, heterotopic bone, and infection).

Intra-articular etanercept attenuates pain and hypoxia from TMJ loading in the rat.

Mechanical overloading of the temporomandibular joint (TMJ) and biochemical changes, like inflammation and hypoxia, contribute to cartilage degeneration and pain associated with osteoarthritis (OA). Yet, how overloading contributes to early dysregulation of chondrocytes is not understood, limiting the development of diagnostics and treatments for TMJ OA. Hypoxia-inducible factors (HIF)-1α/2α in chondrocytes were evaluated at Days 8 and 15 in a rat TMJ pain model induced by jaw loading (1 h/day for 7 days) using immunohistochemistry and compared between cases that induce persistent (3.5 N), acute (2 N), or no (0 N) sensitivity. Hypoxia was measured on Day 8 by immunolabeling of the tracer EF5 and 18 F-EF5 PET imaging. To assess the role of tumor necrosis factor (TNF) in painful TMJ loading, intra-articular etanercept was given before loading. Orofacial sensitivity was evaluated during and after loading. Facial grimace, TNF-α, HIF-2α, and hypoxia levels in the TMJ were measured after loading. HIF-2α was elevated (P = .03) after 3.5 N loading at Day 8, but HIF-1α was unchanged. EF5 uptake increased on Day 8 in the 3.5 N group (P < .048) by tissue assay and 18 F-EF5 PET. At Day 8, both HIF-2α (P = .01) and EF5 uptake (P = .005) were correlated with loading magnitude. Etanercept attenuated sensitivity (P < .01) and the facial grimace on Day 7 (P = .01). It also reduced (P < .01) HIF-2α and EF5 uptake on Day 8; but TNF-α levels were not different from controls at that time. Findings suggest that TMJ loading that induces persistent sensitivity upregulates the catabolic factor HIF-2α and reduces oxygen levels in the cartilage, which may be TNF-driven.

Variability in the Analgesic Response to Ibuprofen Is Associated With Cyclooxygenase Activation in Inflammatory Pain.

The mechanisms underlying interindividual variability in analgesic efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) are not well understood. Therefore, we performed pain phenotyping, functional neuroimaging, pharmacokinetic/pharmacodynamic assessments, inflammation biomarkers, and gene expression profiling in healthy subjects who underwent surgical extraction of bony impacted third molars and were treated with ibuprofen (400 mg; N = 19) or placebo (N = 10). Analgesic efficacy was not associated with demographic or clinical characteristics, ibuprofen pharmacokinetics, or the degree of cyclooxygenase inhibition by ibuprofen. Compared with partial responders to ibuprofen (N = 9, required rescue medication within the dosing interval), complete responders (N = 10, no rescue medication) exhibited greater induction of urinary prostaglandin metabolites and serum tumor necrosis factor-α and interleukin 8. Differentially expressed genes in peripheral blood mononuclear cells were enriched for inflammation-related pathways. These findings suggest that a less pronounced activation of the inflammatory prostanoid system is associated with insufficient pain relief on ibuprofen alone and the need for additional therapeutic intervention.

Prevention of Opioid-Induced Nausea and Vomiting During Treatment of Moderate to Severe Acute Pain: A Randomized Placebo-Controlled Trial Comparing CL-108 (Hydrocodone 7.5 mg/Acetaminophen 325 mg/Rapid-Release, Low-Dose Promethazine 12.5 mg) with Conventional Hydrocodone 7.5 mg/Acetaminophen 325 mg.

OBJECTIVES: To evaluate the prevention of opioid-induced nausea and vomiting (OINV) and the relief of moderate to severe acute pain by CL-108, a novel drug combining a low-dose antiemetic (rapid-release promethazine 12.5 mg) with hydrocodone 7.5 mg/acetaminophen 325 mg (HC/APAP) was used. METHODS: This was a multicenter, randomized, double-blind, placebo- and active-controlled multidose study. After surgical extraction of two or more impacted third molar teeth (including at least one mandibular impaction), 466 patients with moderate to severe pain (measured on a categorical pain intensity scale [PI-CAT]) were randomized to CL-108, HC/APAP, or placebo. Over the next 24 hours, patients used the PI-CAT to assess pain at regular intervals whereas nausea, vomiting, and other opioid-related side effects were also assessed prospectively. Study medications were taken every four to six hours as needed; supplemental rescue analgesic and antiemetic medications were permitted. Co-primary end points were the incidence of OINV and the time-weighted sum of pain intensity differences over 24 hours (SPID24). RESULTS: Relative to HC/APAP treatment alone, CL-108 treatment reduced OINV by 64% (P < 0.001). Treatment with CL-108 significantly reduced pain intensity compared with placebo (SPID24 = 16.2 vs 3.5, P < 0.001). There were no unexpected or serious adverse events. CONCLUSIONS: CL-108 is a safe and effective combination analgesic/antiemetic for the prevention of OINV during treatment of moderate to severe acute pain.

Grading facial expression is a sensitive means to detect grimace differences in orofacial pain in a rat model.

Although pre-clinical models of pain are useful for defining relationships between biological mechanisms and pain, common methods testing peripheral sensitivity do not translate to the human pain experience. Facial grimace scales evaluate affective pain levels in rodent models by capturing and scoring spontaneous facial expression. But, the Rat Grimace Scale (RGS) has not assessed the common disorder of temporomandibular joint (TMJ) pain. A rat model of TMJ pain induced by jaw loading (1 hr/day for 7 days) was used to investigate the time course of RGS scores and compare them between different loading magnitudes with distinct peripheral sensitivity profiles (0N-no sensitivity, 2N-acute sensitivity, 3.5N-persistent sensitivity). In the 3.5N group, RGS is elevated over baseline during the loading period and one day after loading and is correlated with peripheral sensitivity (ρ = -0.48, p = 0.002). However, RGS is not elevated later when that group exhibits peripheral sensitivity and moderate TMJ condylar cartilage degeneration. Acutely, RGS is elevated in the 3.5N loading group over the other loading groups (p < 0.001). These findings suggest that RGS is an effective tool for detecting spontaneous TMJ pain and that spontaneous pain is detectable in rats that develop persistent TMJ sensitivity, but not in rats with acute resolving sensitivity.

Cardiac Fibroma with Ventricular Tachycardia: An Unusual Clinical Presentation of Nevoid Basal Cell Carcinoma Syndrome.

Pediatric cardiac tumors are rare and often benign with an incidence of approximately 0.03-0.32% and can be associated with genetic conditions. For example, approximately 3% of individuals with nevoid basal cell carcinoma syndrome (NBCCS), also known as Gorlin syndrome, have a cardiac fibroma. NBCCS is also characterized by lamellar or early calcification of the falx, jaw keratocysts, palmar and/or plantar pits, and a predisposition for basal cell carcinomas. Given the management implications of NBCCS, including appropriate cancer screenings and precautions, prompt identification of affected individuals is critical. We report a case of a 6-year-old female presenting with ventricular tachycardia secondary to cardiac fibroma. After diagnosis of recurrent jaw keratocysts, she was clinically and molecularly diagnosed with NBCCS. Identification of a cardiac fibroma should prompt careful assessment of past medical and family history with consideration of a diagnosis of NBCCS.

Advanced maxillofacial imaging for temporomandibular disorder in special needs patients.

Temporomandibular disorder (TMD) is prevalent in special needs patients. Clinical examination of the temporomandibular joint (TMJ) complex and imaging in this patient population can be challenging due to patient disposition and cooperation. We report a case of a 29-year-old male with neurologic and behavioral special needs who required advanced maxillofacial imaging for a suspected TMD under general anesthesia, which has not been reported previously. This article intends to serve as a resource for health care providers who may encounter similar clinical situations.

Inter-subject FDG PET Brain Networks Exhibit Multi-scale Community Structure with Different Normalization Techniques.

Inter-subject networks are used to model correlations between brain regions and are particularly useful for metabolic imaging techniques, like 18F-2-deoxy-2-(18F)fluoro-D-glucose (FDG) positron emission tomography (PET). Since FDG PET typically produces a single image, correlations cannot be calculated over time. Little focus has been placed on the basic properties of inter-subject networks and if they are affected by group size and image normalization. FDG PET images were acquired from rats (n = 18), normalized by whole brain, visual cortex, or cerebellar FDG uptake, and used to construct correlation matrices. Group size effects on network stability were investigated by systematically adding rats and evaluating local network connectivity (node strength and clustering coefficient). Modularity and community structure were also evaluated in the differently normalized networks to assess meso-scale network relationships. Local network properties are stable regardless of normalization region for groups of at least 10. Whole brain-normalized networks are more modular than visual cortex- or cerebellum-normalized network (p < 0.00001); however, community structure is similar at network resolutions where modularity differs most between brain and randomized networks. Hierarchical analysis reveals consistent modules at different scales and clustering of spatially-proximate brain regions. Findings suggest inter-subject FDG PET networks are stable for reasonable group sizes and exhibit multi-scale modularity.

Microbiology Alloplastic Total Joint Infections: A 20-Year Retrospective Study.

PURPOSE: Prosthetic joint infection (PJI) is a rare complication of temporomandibular joint replacement (TJR). This study evaluated TJR PJIs at the authors' institution over a 20-year period, including micro-organisms cultured, antibiotic resistance patterns, and intraoperative protocols of TJR. PATIENTS AND METHODS: Patients were identified using Current Procedural Terminology and International Classification of Diseases, Ninth Revision codes and surgical logs from January 1995 through 2015. Inclusion criteria were adults older than 18 years with previous alloplastic TJR and the presence of infection of the prosthesis at explantation. Exclusion criteria were patients younger than 18 years and who received hemiarthroplasty. Primary outcomes included culture data and antibiotic selection for PJI. Secondary outcomes included intraoperative duration and in vivo duration. RESULTS: Eleven patients were identified and 15 joints were explanted. Average length in vivo was 232 months (standard deviation, 478.9 months). Six percent (n = 1) were identified as early PJI (0 to 3 months), 46% (n = 7) were intermediate PJI (3 months to 2 yr), and 33% (n = 5) were late PJI (>2 yr). One patient could not be classified as early, intermediate, or late. Staphylococcus aureus was present in 53% of patients and was the predominant organism isolated. Propionibacterium acnes was isolated in 33% of patients. Penicillin was the antibiotic with the greatest organism resistance (46%). CONCLUSION: In the present study, the most commonly cultured organism was S aureus (53%), a finding consistent with current literature. The prevalence of P acnes colonization was noted in 33% of cases. Although the relevance of P acnes and its contribution to PJI requires further investigation, it is associated with PJI and biofilm formation. Based on this study, consideration could be given to the use of vancomycin and first-generation cephalosporins as perioperative antibiotic coverage.

Odontogenic sinusitis: developments in diagnosis, microbiology, and treatment.

PURPOSE OF REVIEW: Odontogenic causes of sinusitis are frequently missed; clinicians often overlook odontogenic disease whenever examining individuals with symptomatic rhinosinusitis. Conventional treatments for chronic rhinosinusitis (CRS) will often fail in odontogenic sinusitis. There have been several recent developments in the understanding of mechanisms, diagnosis, and treatment of odontogenic sinusitis, and clinicians should be aware of these advances to best treat this patient population. RECENT FINDINGS: The majority of odontogenic disease is caused by periodontitis and iatrogenesis. Notably, dental pain or dental hypersensitivity is very commonly absent in odontogenic sinusitis, and symptoms are very similar to those seen in CRS overall. Unilaterality of nasal obstruction and foul nasal drainage are most suggestive of odontogenic sinusitis, but computed tomography is the gold standard for diagnosis. Conventional panoramic radiographs are very poorly suited to rule out odontogenic sinusitis, and cannot be relied on to identify disease. There does not appear to be an optimal sequence of treatment for odontogenic sinusitis; the dental source should be addressed and ESS is frequently also necessary to alleviate symptoms. SUMMARY: Odontogenic sinusitis has distinct pathophysiology, diagnostic considerations, microbiology, and treatment strategies whenever compared with chronic rhinosinusitis. Clinicians who can accurately identify odontogenic sources can increase efficacy of medical and surgical treatments and improve patient outcomes.

Treatment of the Temporomandibular Joint in a Child with Juvenile Idiopathic Arthritis.

The oral and maxillofacial surgeon is instrumental in the management and care of pediatric patients with juvenile idiopathic arthritis (JIA) and should include JIA in the differential when evaluating pediatric patients with temporomandibular joint (TMJ) dysfunction. Medical management has largely decreased the need for surgical intervention, but these patients may require intraarticular steroid injections of the TMJ, close follow-up to monitor their facial growth, and management of the subsequent postinflammatory degenerative TMJ changes. This article reviews the oral and maxillofacial surgeon's role in the care of patients with JIA involvement in the TMJ.

Development of a Rat Model of Mechanically Induced Tunable Pain and Associated Temporomandibular Joint Responses.

PURPOSE: Although mechanical overloading of the temporomandibular joint (TMJ) is implicated in TMJ osteoarthritis (OA) and orofacial pain, most experimental models of TMJ-OA induce only acute and resolving pain, which do not meaningfully simulate the pathomechanisms of TMJ-OA in patients with chronic pain. The aim of this study was to adapt an existing rat model of mechanically induced TMJ-OA, to induce persistent orofacial pain by altering only the jaw-opening force, and to measure the expression of common proxies of TMJ-OA, including degradation and inflammatory proteins, in the joint. MATERIALS AND METHODS: TMJ-OA was mechanically induced in a randomized, prospective study using 2 magnitudes of opening loads in separate groups (ie.,. 2-N, 3.5-N and sham control [no load]). Steady mouth opening was imposed daily (60 minutes/day for 7 days) in female Holtzman rats, followed by 7 days of rest, and orofacial sensitivity was measured throughout the loading and rest periods. Joint structure and extent of degeneration were assessed at day 14 and expression of matrix metalloproteinase-13 (MMP-13), hypoxia-inducible factor-1α (HIF-1α), and tumor necrosis factor-α (TNF-α) in articular cartilage was evaluated by immunohistochemistry and quantitative densitometry methods at day 7 between the 2 loading and control groups. Statistical differences of orofacial sensitivity and chondrocyte expression between loading groups were computed and significance was set at a P value less than .05. RESULTS: Head-withdrawal thresholds for the 2 loading groups were significantly decreased during loading (P < .0001), but that decrease remained through day 14 only for the 3.5-N group (P < .00001). At day 14, TMJs from the 2-N and 3.5-N groups exhibited truncation of the condylar cartilage, typical of TMJ-OA. In addition, a 3.5-N loading force significantly upregulated MMP-13 (P < .0074), with nearly a 2-fold increase in HIF-1α (P < .001) and TNF-α (P < .0001) at day 7, in 3.5-N loaded joints over those loaded by 2 N. CONCLUSION: Unlike a 2-N loading force, mechanical overloading of the TMJ using a 3.5-N loading force induced constant and nonresolving pain and the upregulation of inflammatory markers only in the 3.5-N group, suggesting that these markers could predict the maintenance of persistent orofacial pain. As such, the development of a tunable experimental TMJ-OA model that can separately induce acute or persistent orofacial pain using similar approaches provides a platform to better understand the pathomechanisms involved and possibly to evaluate potential treatment strategies for patients with painful TMJ-OA.

Retrospective study of facial nerve function following temporomandibular joint arthroplasty using the endaural approach.

The aim of this retrospective case-control study is to evaluate the incidence of facial nerve injury associated with temporomandibular joint (TMJ) arthroplasty using the endaural approach for the treatment of TMJ pathology. The sample consisted of 36 consecutive patients who underwent TMJ arthroplasty. A total of 39 approaches were performed through an endaural incision. Patients undergoing total joint replacement and/or with preexisting facial nerve dysfunction were excluded from the study. Five patients were lost to follow-up and were excluded from the study. Facial nerve function of all patients was clinically evaluated by resident physicians preoperatively, postoperatively, and at follow-up appointments. Facial nerve injury was determined to have occurred if the patient was unable to raise the eyebrow or wrinkle the forehead (temporalis branch), completely close the eyelids (zygomatic branch), or frown (marginal mandibular branch). Twenty-one of the 36 patients or 22 of the 39 approaches showed signs of facial nerve dysfunction following TMJ arthroplasty. This included 12 of the 21 patients who had undergone previous TMJ surgery. The most common facial nerve branch injured was the temporal branch, which was dysfunctional in all patients either as the only branch injured or in combination with other branches. By the 18th postoperative month, normal function had returned in 19 of the 22 TMJ approaches. Three of the 22 TMJ approaches resulted in persistent signs of facial nerve weakness 6 months after the surgery. This epidemiological study revealed a low incidence of permanent facial nerve dysfunction. A high incidence of temporary facial nerve dysfunction was seen with TMJ arthroplasty using the endaural approach. Current literature reveals that the incidence of facial nerve injury associated with open TMJ surgery ranges from 12.5 to 32%. The temporal branch of the facial nerve was most commonly affected, followed by 4 of the 22 approaches with temporary zygomatic branch weakness. Having undergone previous TMJ surgery did not increase the incidence of facial nerve injury using the endaural approach. This information is important for patients and surgeons in the postoperative period, as a majority of patients will experience recovery of nerve function.