fmictafmo

aDThs

Risk Factors in the Initiation ofCondylar ResorptionG. William Arnett, DDS, FACD,* and Michael J. Gunson, DDS, MD**

Progressive condylar resorption is a process that involves the temporoman-

dibular joint (TMJ) and the occlusion. During growth, condylar resorption

may decrease the projection of the mandible and be unrecognized as the

source of a Class II malocclusion. After growth completion, as the condyle

resorbs, the occlusion becomes progressively Class II, with or without open

bite. Broadly speaking, condylar resorption is initiated or maintained by a

combination of systemic factors and any form of TMJ compression, includ-

ing pressure resulting from dental treatment. (Semin Orthod 2013;19:81-88.)

© 2013 Published by Elsevier Inc.

gmp

dat(sc

ioa(

T wo distinct categories of temporomandibu-lar joint (TMJ) remodeling can occur:

unctional remodeling and dysfunctional re-odeling.1-6 Functional remodeling of the TMJ

s an ongoing process involving morphologichanges of the articular structures of the jointhat are not associated with any significant alter-tions in the joints or the occlusion. Therefore,unctional remodeling is characterized by TMJ

orphologic change, stable ramus height, stablecclusion, and normal growth.

Remodeling of the TMJ is dysfunctional if itdversely affects the joints and the occlusion.ysfunctional remodeling is distinguished byMJ morphologic change (decreased condylaread volume), decreased ramus height, progres-ive mandibular retrusion (adult), or decreased

*Goleta Valley Cottage Hospital, Santa Barbara, CA; VisitingProfessor, Universidad del Desarrollo, School of Dentistry, Faculty ofMedicine, Santiago, Chile; Clinical Assistant Professor, Universityof Southern California, School of Dentistry, Los Angeles, CA; Assis-tant Professor, Loma Linda University, Department of Orthodontics,Loma Linda, CA; Senior Lecturer, Department of Oral and Max-illofacial Surgery, School of Dentistry, University of California at LosAngeles, Los Angeles, CA. **Goleta Valley Cottage Hospital, SantaBarbara, CA. Santa Barbara Cottage Hospital, Santa Barbara, CA.International University of Catalonia, Department of Oral andMaxillofacial Surgery, Barcelona, Spain.

Address correspondence to G. William Arnett, DDS, FACD,Arnett Gunson Facial Reconstruction, 9 East Pedregosa Street,Santa Barbara, CA 93101. E-mail: Arnett@arnettgunson.com.

© 2013 Published by Elsevier Inc.1073-8746/13/1902-0$30.00/0

http://dx.doi.org/10.1053/j.sodo.2012.11.001

Seminars in Orthodontics, Vol 19,

rowth rate (juvenile). This negative type of re-odeling is often described as progressive/idio-

athic condylar resorption.The effects of dysfunctional remodeling (con-

ylar resorption) on adult mandibular positionre clear: as the condyles progressively resorb,he mandible progressively retrudes. The causecondylar resorption) and the effect (progres-ive mandibular retrusion) are undeniably andlearly linked.1-6

The effects of dysfunctional remodeling (con-dylar resorption) on the growing mandible arealso clear. If it occurs during growth, condylarresorption decreases the condylar size and themandibular growth rate, resulting in mandibu-lar retrusion. The condylar growth is diminishedby negative remodeling, and the mandible in-creasingly becomes Class II, with lack of fullforward growth.1-6 Therefore, factors that dimin-sh the functional condylar remodeling capacityr increase the compression on the TMJ maydversely alter condylar size and the occlusionFig 1).

Host Remodeling Capacity

Age, gender, systemic illnesses, and hormonalfactors may influence the host adaptive capacityof the TMJ.1-6

1. Age and gender—Condylar resorption ismore prevalent in younger age-groups, espe-

cially among female individuals, and the rea-

81No 2 (June), 2013: pp 81-88

2

82 Arnett and Gunson

sons for these differences in prevalence areunclear.

. Systemic illnesses—These illnesses may in-clude autoimmune disorders, endocrine dis-orders, nutritional disorders, and metabolicdiseases. In particular, autoimmune diseaseshave been associated with condylar resorp-tion in numerous publications, as summa-rized by Arnett et al.1-6

3. Hormones—Hormonal factors may have amarked influence on regressive remodelingof the mandibular condyle. Among them are

Figure 1. Condylar resorption (center) is a result ofTMJ inflammation (white). Inflammation is the sumof joint compression (gray left) and systemic overlay(gray right). Systemic factors (black right), includingillnesses, hormonal imbalance, age, and gender, mayupmodulate systemic inflammation, which, in turn,upmodulates resorption. Additionally, compression(gray left), when present, upmodulates compressiveinflammation, which, in turn, increases condylar re-sorption. Compression (gray left) is the sum of activefactors (black left), which may include unstable occlu-sion, parafunction, bite correction, condylar displace-ment, internal derangement, and isolated macro-trauma. To decrease the risk of bite treatment causingcondylar resorption, techniques should be used thatavoid condylar displacement. Most importantly, in thecourse of performing orthognathic surgery, surgicaltechniques are used to decrease treatment compres-sion. Medications inhibit or control inflammation andcondylar resorption from either compressive or sys-temic origins.

the following:

a. Low estrogen: Arnett and Tamborello havereported observations about a group offemale idiopathic condylar resorption pa-tients.1,6 Examination of this group re-vealed progressive bilateral condylar re-sorption leading to progressive Class IImalocclusions. Recently, Gunson et al.6 re-ported 27 female idiopathic condylar re-sorption patients who all had low estrogenlevels, indicating a possible cause (low es-trogen) and effect (condylar resorption).These clinical experiences indicate thatsome females may be predisposed to dys-functional remodeling of the TMJ in re-sponse to loading associated with occlusaltreatment. This apparent female prepon-derance for dysfunctional remodeling ofthe TMJ suggests a potential role of sexhormones as modulators of this response(Fig 2).

b. Prolactin: Prolactin, a hormone responsiblefor initiating postpartum milk letdown,can exacerbate cartilage and bone degra-dation in animal models of inflammatoryarthritides. It is likely that prolactin con-tributes to the accelerated condylysis thathas been observed in some pregnantwomen. It appears that female predisposi-tion to dysfunctional remodeling of theTMJ may be attributed, in part, to themodulation of the biological responses ofarticular tissues to joint loading by sex hor-mones. Other factors that contribute tothe sex-based predilection to dysfunctionalremodeling of the TMJ may be identifiedin the future.

c. Corticosteroids: Corticosteroids have beenreported as causing joint resorption. It isconceivable that changes in corticosteroidlevels may, in some individuals, initiatemandibular condylar resorption and atten-dant progressive Class II malocclusion.2-5

Mechanical Compression Factors

Temporomandibular joint loading producescompressive forces that provoke molecular andsoft-tissue adaptive remodeling responses in thenormal TMJ.1-12 Ultimately, under unusual com-pressive loads, joint soft-tissue changes may con-tribute to functional or dysfunctional osseous

remodeling. Multiple animal studies have as-

owc

carfS

oaflcc

ay.

83Initiation of Condylar Resorption

sessed the osseous changes that have been asso-ciated with condylar displacement. These studieshave shown consistent osseous resorption of thepostglenoid spine and posterior condylar sur-face when the condyle is posteriorly displacedand compressed in the glenoid fossa. A summaryof compression studies has been published byArnett et al.2-5 Similarly, Arnett11,12 and Tambo-rello11 have demonstrated morphologic changes

f the human mandibular condyle associatedith posteriorization and/or medial or lateralondylar torquing during orthognathic surgery.

Mechanical factors that can cause changes inondylar morphology2-12 include occlusal ther-py, internal derangement, parafunction, mac-otrauma, and unstable occlusion; each of theseactors is discussed in detail later in the text.

Figure 2. Factors that increase joint compression (utrauma, and internal derangement) and/or diminisimbalance, young age, and gender) of the TMJ mayocclusal correction. Head film and left sagittal tomoorthognathic surgery (pre), (B) 7 months after orthsurgery. Note the extreme dysfunctional remodelingdysfunctional condylar resorption resulted in a ClaDysfunctional condylar resorption is the sum of hiddein this case). History, examination, and blood work revsyndrome—hidden systemic factor), which led to psurgery. During this procedure, normal orthognathic swas designed to produce minor joint compression.profound resorption secondary to low estrogen overl

uch mechanical factors may occur in isolation,

r they may be interrelated, interdependent,nd coexistent. When 2 or more biomechanicalactors coexist, morphologic change is moreikely to occur. Additionally, if the host adaptiveapacity is limited, morphologic changes are ac-entuated when compression factors are active.

TMJ Remodeling in Response to OcclusalCorrection Procedures

Animal studies, as summarized by Arnett et al,2-5,11,12

have shown that, in every instance, suddenchange of the mandibular condyle position sec-ondary to occlusal change leads to postglenoidspine and posterior condylar resorption.

In addition, as summarized by Arnett et al,2-5,11,12

orthodontics, prosthetics, and orthognathic

ble occlusion, parafunction, bite correction, macro-e remodeling capacity (systemic illnesses, hormonale condylar resorption and mandibular relapse afters are depicted for a 21-year-old woman. (A) Beforethic surgery, and (C) 34 months after orthognathiccted in the tomograms from (A) to (B) to (C). Theocclusion with anterior open bite (C, head film).

temic factors and compression (orthognathic surgeryd that the patient did not produce estrogen (Kallmanund condylar resorption after normal orthognathicry (standard techniques) as performed by the authorsite minor compression, the patient responded with

nstah thcaus

gramognadepiss IIn sysealerofourgeDesp

surgery can produce condyle remodeling or

84 Arnett and Gunson

resorption resulting from displacement andcompression during treatment; these changesmay be either functional, maintaining theocclusion, or dysfunctional, with attendantClass II malocclusion development. Coexistingremodeling stimuli (internal derangement,parafunction, macrotrauma, unstable occlu-sion, hormones, or systemic diseases) may ac-centuate condylar remodeling and produce adysfunctional Class II malocclusion.-12

During most orthognathic surgery proce-dures, gross positional changes of the mandibu-lar condyle can occur, so those procedures havea high risk of producing gross condylar morpho-logic changes.11,12 Arnett and Tamborello11,12

studied the TMJ tomograms from 61 orthog-nathic surgery patients to determine the effectsof surgically induced condylar position changeon the morphology of the mandibular condyle.They found that intraoperative condylar torqu-ing or posteriorization leads to condylar resorp-tion and late mandibular relapse.11,12

Orthodontic and prosthetic occlusal treatmentmay also produce condyle position changes, butgenerally not to the same extent and not as sud-denly as orthognathic surgery. Therefore, thesenonsurgical procedures can contribute to signifi-cant condylar remodeling, especially in susceptibleindividuals with concurrent predisposing compres-sive and/or systemic overlays. Class II orthodonticpatients seem to be particularly susceptible to con-dylar displacement, perhaps because predisposingcompressive and systemic factors may be thesource of the original Class II malocclusion.

Articular Disk Displacement(Internal Derangement)

The relationship between internal derangement(ID) and condylar remodeling in adults is notwell understood. Arnett et al2-5 have summarizedthe internal derangement literature, with a spe-cial focus on the relationship between ID andcondylar resorption. ID is very common in thepopulation, and is found with and without bonyTMJ remodeling. Thus, there does not seem tobe a clear cause-and-effect relationship betweenID and shape changes of the condyle and fossain adult patients.

In the growing patient, ID is suspected ofdiminishing condylar growth, thereby negatively

affecting mandibular growth. It is possible that

when ID exists, the anterior growth of the man-dible is reduced. However, patients with mandib-ular deficiency commonly have normal disk po-sition, and patients with normal mandibulargrowth commonly have ID. As a result, currentlyno cause-and-effect relationship can be deter-mined for anterior disk position and mandibulargrowth deficiency.2-5

When ID and condylar remodeling do occurconcurrently, the ID may produce condylar re-modeling by contributing to compressive load-ing of articular tissues. This notion is supportedby multiple studies showing that condylar re-modeling is more likely to be associated withnonreducing disk displacement cases than withreducing (clicking) disks.2-5

Parafunction

Parafunction may produce joint compressionthat can enhance resorption caused by otherfactors that initiate this process. Parafunction isparticularly destructive when combined withcondylar displacement associated with orthog-nathic surgery or other major occlusal treatmentmodalities.2-5 In such cases, parafunction mayincrease intracapsular pressures and inhibit cap-illary perfusion, thereby producing an ischemicinjury with attendant loss of temporomandibulartissue volume leading to mandibular retrusion.

Macrotrauma

Macrotrauma to the face may initiate condylarresorption. Macrotrauma consists of one epi-

Table 1. List A: Condyle (1-7) and List B: Fossa (1-5)

Normal CR

A Condylea

1. Head bulge Yes No2. Size Normal Small3. Surface contour Rounded Flat surface4. Spurs No Variable5. Cortex irregular No Yes6. Cortex breaks No Yes7. Subcortical cysts No Variable

B Fossab

1. Depth Variable Variable/shallow2. Surface contour Rounded Flat surface3. Cortex irregular No Yes4. Cortex breaks No Yes5. Subcortical cysts No Yes

aCone beam computed tomography (CT) condyle character-istics associated with a normal condyle and CR are listed.b

Cone beam CT fossa characteristics associated with a nor-mal joint and condylar resorption joint (CR) are listed.

85Initiation of Condylar Resorption

sode of large-magnitude force that is transmittedto articular structures of the temporomandibu-lar joint. The force is generally of a sufficientmagnitude that it is acutely injurious to affectedarticular tissues. The occlusion is not altered at thetime of the macrotrauma, but TMJ alterations canoccur over time after the macrotrauma, leading toprogressive mandibular retrusion.

Unstable Occlusion

By definition, a stable occlusion is produced whenthe teeth maximally intercuspate under muscleforce and the condyle is not displaced and/orcompressed. When a stable occlusion exists, thejoints and the occlusion do not change signifi-cantly over time. Most natural occlusal relation-ships between maxillary and mandibular teeth arestable, regardless of the Angle classification. This istrue because teeth and TM joints develop anongoing noncompressed homeostatic relation-ship, and therefore, it is unlikely that there willbe strong compressive forces acting on the TMJin such stable occlusions. By definition, an un-stable occlusion is produced when the teeth in-tercuspate under muscle force and the condyleis displaced and/or compressed. The com-pressed joint position then causes some degreeof remodeling to occur, depending on the mag-nitude of position change and coexistent sys-temic factors. As stated earlier in the text, con-dylar displacement and compression may occurduring occlusal correction procedures as simple

Figure 3. The cone-beam computed tomography(CT) images of a normal right TMJ is shown. Normaljoints have condylar head bulge (condyle larger thanneck), rounded surfaces, smooth and continuous cor-tex, and no subcortical cysts.

as splint therapy or restorative procedures and

as complex as orthognathic surgery. However,unstable occlusions also can be produced bynontreatment compressive etiologies such asheavy joint loading (bruxism, clenching) or diskderangements, combined with underlying sys-temic factors (low estrogen, rheumatoid arthri-tis, etc). These nontreatment factors can initiatethe unstable occlusion, and then the unstableocclusion produces increased compression, re-sorption, and increased mandibular relapse. Un-

Figure 4. The cone-beam CT images of the right(above) and left (below) TMJ of the same patient onthe same day are displayed. The right joint showsevidence of past change as indicated by lack of headbulge, small size, a medial spur, and flat superiorsurface. Additionally, the right joint demonstrates ac-tive changes, including condylar and fossa corticalirregularity, cortical breaks, and a singular subcorticalbone cyst in sagittal view. The left TMJ (below) dem-onstrates normal size and shape, indicating thatchange has not occurred in the past. However, evenwithout past left joint change, the cortex indicatesthat the joint is actively changing, as indicated bycortical irregularity, cortical breaks, and subcorticalbone cysts. Both joints are in the in the process ofcondylar resorption, the right preceding the left. Thehead film and frontal bite photo for this patient are in

shown in Figure 5.

scfOpttsdlwo

86 Arnett and Gunson

der unstable condylar conditions, the condylesare displaced by the malocclusion, thereby cre-ating a cycle of compression and resorption un-til a stable occlusion is produced and/or cofac-tors such as low estrogen, rheumatoid arthritis,and so forth are controlled.

Control of Condylar ResorptionAssociated With Occlusal Treatment

Condylar and fossa characteristics for a normaljoint and a condylar resorption (CR) joint areshown in Table 1. A normal joint has a condylarhead larger than the neck (head bulge), normalsize, and rounded surfaces of the condyle andfossa (Fig 3). Shape changes (Fig 4) generallyindicate changes that have occurred in the past;however, these changes may be ongoing as well.Shape changes may include some or all the fol-lowing: small condyle, no head bulge, flat sur-faces, and spurring. The fossa shape changesinclude flat surfaces and shallowness. Changesin the cortex (Fig 4) of the condyle and fossaindicate that condylar resorption is active, whichproduces breaks in the cortex, cortex irregular-ity, and subcortical cysts of the condyle andfossa. The facial skeleton is affected by condylarresorption. If both TM joints resorb symmetri-cally, the facial skeleton demonstrates a high-angle Class II malocclusion. If only one jointresorbs, or if one precedes the other, the man-

Figure 5. The head film and frontal cone-beam CT imII anterior open bite malocclusion. The etiology for tsive and systemic overlay factors. Note that the mand

canted up, both findings related to the smaller right joint

dible deviates to the smallest joint and cants upon the small side (Fig 5).

When active bilateral condylar resorption isidentified or suspected, a rheumatology referralis indicated with appropriate laboratory studies(Table 2) to rule out collagen vascular disorderssuch as rheumatoid arthritis. Stabilization ofprogressive condylar resorption cases may beachieved with control of preexisting compressivefactors, systemic factors, and the biological deg-radation caused by both, and this should bedone before initiating any corrective surgicalprocedures. Medications7,14,15,16 (Table 3) andplint therapy are commonly used before surgi-al occlusal correction, and may be appropriateor other occlusal correction techniques as well.ne thing that has been learned from our ex-eriences with progressive condylar resorption ishat occlusal treatment techniques to minimizehe possibility of compression-related resorptionhould be used—even if condylar resorptionoes not exist. Quite stable joints can be stimu-

ated to resorb if treatment compresses the jointhile producing bite correction, especially withrthognathic surgery.

Surgical Management Concepts and Procedures

Arnett and Gunson have presented surgicaltechniques to limit surgical compression andresultant condylar resorption. These sagittal

s of the patient in Figure 4 are shown. Note the Classalocclusion is indeterminate but related to compres-ar midline is to the right and the right mandible is

agehis mibul

. (Color version of figure is available online.)

ebgpddhu

mtaratilRb((F

MrtcemtitWF

87Initiation of Condylar Resorption

osteotomy techniques include bivector condy-lar seating, no segment clamping, no bicorti-cal screws, plate fixation, a short split, osteot-omy stretch, and anterior bone anchorplacement. Postsurgical techniques includemedications as needed, opening exercises,Class II elastics, and anterior skeletal elas-tics.11-13 Condylar torque is associated withsegment clamping and bicortical screw fixa-tion of bilateral sagittal osteotomy surgery.11-13

Joss and Vassalli17 reviewed the literature com-paring stability of sagittal osteotomy advance-ments when bicortical screws or miniplateswere used. He found much greater long-termrelapse (condylar resorption) for cases treatedwith bicortical screws (2%-50.3%), whereasminiplates had comparatively much less re-lapse (1.5%-8.9%).

Additionally, Gunson and Arnett7,15 havesuggested medical management to stabilizethe biology of resorption initiated by inadver-tent treatment compression of the TMJ or sys-temic diseases (Fig 5). The cellular pathwaysfor bone loss at the mandibular condyle re-quire specific cytokines and enzymes. If thosecytokines and enzymes are blocked, condylarresorption is minimized or eliminated in spiteof systemic factors or compression. Tumor ne-crosis factor-alpha (TNF-�) is a known cyto-kine that promotes osteoclastogenesis and

Table 2. Basic Laboratory Studies to IdentifySystemic Arthritides are Listed

1 RF—rheumatoid factorElevated 80% correlation with RA

2 Anti-CCP—anti-cyclic citrullinated peptide antibody90%-95% correlation with rheumatoid arthritis (RA)Reveals RA earlier than RFMore specific to RA than RF

3 ANA—antinuclear antibodyAssociated with autoimmune disorders, infections,

cancer25%-30% RA have positive ANA

4 Sed rate—erythrocyte sedimentation rateIndicates inflammatory activity

5 CRP—C-reactive proteinGeneral marker of inflammationMay elevate with RA

6 25-Hydroxyvitamin DDeficiency associated with osteoporosisDeficiency secondary to low sunlight exposure or

decreased dietary intake7 17�-Estradiol

Maintenance of boneLow estradiol associated with osteopenia and porosis

osteoclast activity in the joints of patientstt

with inflammatory arthritis. By administeringTNF-� inhibitors (etanercept, adalimumab,tc), bone loss at the mandibular condyle maye controlled before, during, and after sur-ery. Another example is the matrix metallo-roteinase (MMP) enzymes, which breakown collagen as the final step in articularestruction. Tetracyclines are known MMP in-ibitors and have been shown to reduce artic-lar erosions in susceptible patients.

We believe that medical and compressiveanagement of the TMJ significantly reduces

he need for total TM joint replacement therapy;similar shift is occurring in regard to total hip

eplacement surgery as reported by Hekmat etl.16 They state that “Potential explanations forhe reduced rate of total hip arthroplasty (THA)nclude reduced rheumatoid arthritis (RA) re-ated joint damage due to better management ofA.” In their study, Hekmat et al found thatoth disease-modifying antirheumatic drugDMARD) (52%-87%) and TNF-inhibitor drug0%-20%) use has increased from 1997 to 2005.urthermore, Hekmat states, “There is extensive

Table 3. Medications Used to Control TMJ Arthritis

Vit D and Ca�� Bone densityC 500 mg and E 400 u AntioxidantsOmega-3 fatty acid 2-4 G Potent antioxidantDoxycycline, 50-100 mg Anti-inflammatory, MMP,

cytokine inhibitorFeldene, 10-20 mg Anti-inflammatory, MMP,

cytokine inhibitorSimvastatin, 20 mg Anti-inflammatory, MMP,

cytokine inhibitorCelebrex, 100 mg Anti-inflammatory, MMP,

cytokine inhibitorAmitriptyline, 5-15 mg Antibruxism, mm relaxKlonapin, 0.5-1 mg AntibruxismTiagabine, 2-4 mg AntibruxismBotox injection, 36-48 u AntibruxismSimvistatin, 20 mg Autoimmune inhibitor17�-Estradiol, variable Potent anti-inflammatoryEtanercept, 50 mg q week TNF-� inhibitorAdalimumab, 40 mg q 2

weeksTNF-� inhibitor

edications are used to control the biology of condylaresorption whether secondary to compression and/or sys-emic overlay, whether before or after treatment when activeondylar resorption is occurring. All medications and gen-ral dosages are listed on left. The biological effects of eachedication are listed on the right. Each patient generally will

ake vitamin D, calcium, doxycycline, and Feldene. If brux-sm is a component of loading, one of the bruxism medica-ions will be selected until control of symptoms is achieved.

hen resorption is active and aggressive as indicated inigure 1 earlier in the text, additional appropriate medica-ions are added, including an autoimmune inhibitor and, in

he case of low estrogen, 17�-estradiol.

1

1

1

1

1

1

1

1

88 Arnett and Gunson

evidence for a reduced peripheral joint damagein patients with RA treated with TNF inhibitors,and such treatment could also prevent hip de-struction.” The parallels to the temporomandib-ular joint should be obvious, and it is our hopethat this more conservative viewpoint becomeswidely accepted in our field.

References1. Arnett GW, Tamborello JA: Progressive class II develop-

ment—Female idiopathic condylar resorption, in WestRA (ed): Oral and Maxillofacial Surgery Clinics of NorthAmerica - Orthognathic Surgery (vol 2). Philadelphia,W. B. Saunders, 1990, pp 699-716

2. Arnett GW, Milam SB, Gottesman L: Progressive man-dibular retrusion—Idiopathic condylar resorption. partI. Am J Orthod Dentofacial Orthop 110:8-15, 1996

3. Arnett GW, Milam SB, Gottesman L: Progressive man-dibular retrusion—Idiopathic condylar resorption: PartII. Am J Orthod Dentofacial Orthop 110:117-127, 1996

4. Arnett GW, Milam S: The unfavorable long-term resultin orthognathic surgery II: Injury to the temporoman-dibular joint and trigeminal nerve, in Kaban LB, PogrelMA, Perrott DH (eds): Complications in Oral and Max-illofacial Surgery. Philadelphia, W. B. Saunders Co,1997, 265-277

5. Arnett GW, Milam SB, Gottesman L, et al: Morphologicchanges of the temporomandibular joint associated withorthognathic surgery, in Fonseca RJ (ed): Oral and Max-illofacial Surgery, Orthognathic Surgery. Philadelphia,W. B. Saunders, 2000

6. Gunson MJ, Arnett GW, Formby B, et al: Oral contra-ceptive pill use and abnormal menstrual cycles in womenwith severe condylar resorption: A case for low serum17�-estradiol as a major factor in progressive condylarresorption. Am J Orthod Dentofacial Orthop 136:772-

779, 2009

7. Gunson MJ, Arnett GW, Milam SB: Pathophysiology andpharmacologic control of osseous mandibular condylarresorption. J Oral Maxillofac Surg 70:1918-1934, 2012

8. Arnett GW, Tamborello JA: Condylar movement duringintermaxillary fixation sagittal osteotomy. Clinical Con-gress on Orthognathic Challenges: Predictability, stabil-ity and complications. AAO/AAOMS Clinical Congress,Scientific Abstract Session, 1986

9. Arnett GW, Tamborello JA: TMJ dysfunction from tran-sorally placed lag screws: Fact or fiction? J Oral Maxillo-fac Surg 46:625, 1988

0. Arnett GW: Condylar positioning in orthognathic sur-gery. Round table clinics. J Oral Maxillofac Surg 48(suppl 1):25, 1991

1. Arnett GW, Tamborello JA, Rathbone JA: Temporoman-dibular joint ramifications of orthognathic surgery, inBell WH (ed): Modern Practice in Orthognathic andReconstructive Surgery. Philadelphia, W. B. SaundersCo, 1992, 522-593

2. Arnett GW: A redefinition of bilateral sagittal osteotomy(BSSO) advancement relapse. Am J Orthod DentofacialOrthop 104:506-515, 1993

3. Arnett GW, Gunson MJ: Management of condylar re-sorption before, during, and after orthognathic surgery.Int J Oral Maxillofac Surg 40:1021, 2011

4. Gunson MJ, Arnett GW: Treating severe condylar resorp-tion patients with orthognathic surgery and tumor ne-crosis factor alpha inhibitors. Int J Oral Maxillofac Surg40:1087, 2011

5. Gunson MJ, Arnett GW: Condylar resorption, matrixmetalloproteinases, and tetracyclines. RWISO J 2:37-44,2010

6. Hekmat K, Jacobsson L, Nilsson J-A, et al: Decrease inthe incidence of total hip arthroplasties in patients withrheumatoid arthritis--results from a well defined popu-lation in south Sweden. Arthritis Res Ther 13:R67, 2011

7. Joss CU, Vassalli IM: Stability after bilateral sagittal splitosteotomy advancement surgery with rigid internal fixa-tion: A systematic review. J Oral Maxillofac Surg 67:301-

313, 2009