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xxxvi
Stack BC. My journey from orthodontics to craniofacial pain and TMJ to
movement disorders. Cranio. 2012;30(3):156–8. https://doi.org/10.1179/
crn.2012.023.
Brown JL. Brendan C. Stack, The father of TMJ treatment. Cranio.
2020;38(6):357. https://doi.org/10.1080/08869634.2020.1823792.
BrendanC.Stack Jr.
Acknowledgments

Contents

Part I Fundamentals
The Temporomandibular Joint: Form and Function . . . . . . . . . . . . . 3
Anita R. Joy-Thomas and Robert D. Spears
The Etiology of Temporomandibular Disorders . . . . . . . . . . . . . . . . . 21
Feras Al Khatib and Achint Utreja
Orthodontics and Temporomandibular Disorders . . . . . . . . . . . . . . . 43
Achint Utreja and Feras Al Khatib
An Overview of Chronic Neuropathic Orofacial Pain . . . . . . . . . . . . . 55
Revathi Shekar
Imaging of the Common Conditions of the
Temporomandibular Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
Husniye Demirturk and Anitha Potluri
Temporomandibular Joint: Review of the Anatomy,
Pathology, and Magnetic Resonance Imaging Techniques . . . . . . . . . 91
Francisco Abaete Chagas-Neto, José Luiz de Sá Neto, and Paulo Moraes Agnollitto
Basic Clinical Management of Temporomandibular
Disorders (TMDs) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
Cyril Pandarakalam
Review of TMJ Surgery for Non-surgeons . . . . . . . . . . . . . . . . . . . . . . 135
Ioannis Gkikas
Arthrocentecis and Arthroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
Anis Tebyanian
Part II Advanced Topics
The Neurological Aspects of the Trigeminal Cranial Complex and Its Role in the TMJ Dysfunction and Multiple
Movement Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
Anthony B. Sims
xxxvii
xxxviii
A Journey to Understanding and Treating TMD/Craniofacial Pain: Rediscovering the Structure Often Overlooked
in Orthodontics and Facial Orthopedics: The TMJ . . . . . . . . . . . . . . 185
Lidia Yavich
Structural Misalignment: Postural Changes Related
to Temporomandibular Joint Pathology . . . . . . . . . . . . . . . . . . . . . . . . 205
Lidia Yavich
TMJ Pathology Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
Lidia Yavich
Transformation of Trigeminal Nerve Stimuli into Movement Disorders: A Series of Cases
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Anthony B. Sims
Contents
Part I
Fundamentals
The Temporomandibular Joint: Form andFunction
AnitaR.Joy-Thomas andRobertD.Spears

1 Introduction

The temporomandibular joint (TMJ) is a special­ized synovial joint that is essential for the full range of function of the mammalian jaw. It is a complex joint made up of various tissue types, including bone, cartilage, connective tissues, as well as associated muscles and tendons. The TMJ is described as a bilateral, diarthrodial, synovial joint that is located between the mandibular con­dyles and the temporal bones. Each TMJ is made up of the condylar head of the mandible, the gle­noid fossa and articular eminence of the temporal bone, an articular disc, and a synovial membrane­lined brous capsule that encloses the entire joint (Fig.1). The articulating surfaces of the joint are lined by brocartilage, rather than hyaline carti­lage, in adults. The articular disc is another unique feature of the TMJ, which by its location
divides the joint space into two chambers—supe­rior and inferior (Fig.2). This particular anatomi­cal feature of the TMJ allows the joint to function as a unit in both hinge/axial/rotational (gingly­mus) and gliding/translational (arthrodial) move­ments, thus also being described as a ginglymoarthrodial joint [1, 2].
As with any joint in the human body, the TMJ not only allows for a full range of motion associ­ated with mastication, but it also reduces forces acting on the associated bones by dissipation or distribution of load-bearing from the associated bones to the surrounding soft tissues. TMJ dys­function therefore affects not only the bony com­ponents of the joint, but also the soft tissue components. Therefore, from a functional stand­point and to better manage TMJ dysfunction, a thorough understanding of TMJ anatomy, both of the hard and soft tissue components, is essential.
A. R. Joy-Thomas (*) · R. D. Spears Department of Diagnostic and Biomedical Sciences, UTHealth Houston School of Dentistry, Houston, TX, USA e-mail: Anita.JoyThomas@uth.tmc.edu;
Robert.D.Spears@uth.tmc.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 B. C. Stack Jr. et al. (eds.), Craniofacial Pain, https://doi.org/10.1007/978-3-031-57563-1_1
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A. R. Joy-Thomas and R. D. Spears
Fig. 1 Anatomy of the normal human temporomandibu­lar joint. Photographs of human skulls from a young ado­lescent (a) and an adult (b) show the difference in size of the bony components of the temporomandibular joint. The circled area in both panels shows the condylar head of the
a
b
mandible located posterior to the articular tubercle of the temporal bone. Note the difference in size of the articular tubercle between the adolescent skull and the adult skull. (Anatomical specimen courtesy of Dr. Anita Joy-Thomas,
UTHealth Houston School of Dentistry)
Fig. 2 Coronal section through the temporomandibular joint showing the articular disc and the two joint compart­ments. Image shows a coronal section through a plasti­nated anatomical specimen. The outlined area in panel a is enlarged in panel b and shows the articular disc situated in the joint space. The position of the articular disc divides the joint space into a superior and inferior chamber.
Coronal sections through the condylar head of the man­dible, and three muscles of mastication (masseter, inferior and superior heads of the lateral pterygoid, and supercial and deep heads of the medial pterygoid) are also visible. (Plastinated anatomical specimen courtesy of the
Anatomy Collection at the UTHealth Houston School of Dentistry)
The Temporomandibular Joint: Form andFunction
5

2 Embryology

The embryonic development of the human TMJ follows a similar process that is shared across various mammalian species. However, TMJ development is signicantly different compared to other synovial joints in the body. In long bones, synovial joint formation occurs by carti­laginous differentiation at the locations of the joints, which then undergo cleavage or segmen­tation secondary to cartilage formation. This process occurs through the development of a noncartilaginous region known as the inter­zone, which serves as a critical signaling cen­ter, expressing bone morphogenetic proteins (BMPs), Wnt-14/beta- catenin, as well as BMP antagonists. The interplay between these sig­naling molecules allows for the interzone to maintain its nonchondrogenic nature. Interzone formation is followed by joint cavitation, which is regulated by the nonchondrogenic interzone cells secreting hyaluronan. The articular carti­lage then continues to develop by appositional growth in the long bone [35]. In contrast, dur­ing TMJ development, there are two distinct and unconnected mesenchymal condensations or blastemas that grow toward each other while undergoing different ossication processes that ultimately result in the formation of the man­dibular condyle and the glenoid fossa of the temporal bone. The condylar blastema arises from the secondary condyle cartilage of the mandible and forms bone through endochon­dral ossication. The glenoid fossa blastema arises from the otic capsule and undergoes intramembranous ossication [57]. The gle­noid fossa blastema forms posterior and lateral to the developing condylar blastema. The con­dylar blastema then grows rapidly toward the glenoid fossa blastema, and during this growth, the intervening mesenchyme between the gle­noid fossa and condylar blastemas is trapped, condenses, and differentiates into the lateral pterygoid muscle and the articular disc. This developmental sequence results in the superior belly of the lateral pterygoid muscle having an attachment on the medial aspect of the articular disc in the adult.
Early TMJ development includes the follow­ing stages—(1) blastematic stage (7–9weeks in utero), (2) cavitation stage (9–11weeks in utero), and (3) maturational stage (after 11 weeks in utero). During the blastematic stage is when mes­enchymal condensation of cells occurs at the site of the future condylar cartilage. During this stage, intramembranous ossication of the squamous part of the temporal bone has also begun. During the cavitation stage, chondrocytes are clearly evi­dent in the condylar blastema, and clefting occurs in the area that will form the future joint cham­bers, with the inferior cleft (future inferior joint chamber) forming rst. Development of the TMJ occurs relatively later in utero (about 7–8weeks) unlike most other synovial joints that have com­pleted their initial cavity development by the sev­enth week in utero. In contrast, the TMJ has scarcely begun its development at this time and does not exhibit cavitation until approximately 9–11weeks in utero. By week 13in utero of the maturational stage, the area of the glenoid fossa acquires a clearly concave morphology. After week 14in utero, a clear reduction in the size of Meckel’s cartilage is also evident. It is only after about 18–20weeks in utero that the TMJ is truly functional (i.e., with lateral pterygoid muscle attached to the condyle and the articular disc). After 18–20weeks in utero, the TMJ takes over as the primary joint between the cranium and mandible. Later in the prenatal period, the condy­lar cartilage, which was originally carrot-shaped, gradually thins as birth approaches, and this is accompanied by the presence of vascular ingrowths into the condylar cartilage, a feature that is not seen in other cartilages.
2.1 Role ofMeckel’s Cartilage
In addition to these two mesenchymal condensa­tions that contribute to TMJ development, the Meckel’s cartilage, a primary cartilage derived from the rst branchial arch, is critical in man­dibular formation and growth. However, this car­tilage has no part to play in the formation of the mandibular condyle. The cartilage that forms the condyles develops adjacent to the intramembra-
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A. R. Joy-Thomas and R. D. Spears
Fig. 3 Fate of Meckel’s cartilage. Diagrammatic repre­sentation of the development of the mandible and the role of Meckel’s cartilage. Panel a shows the Meckel’s carti­lage located lateral to the developing mandibular bone. Meckel’s cartilage is continuous on its proximal end with the cartilage that will develop into the malleus and incus, two of the bones found in the middle ear. Panel b shows the mandible at birth. Remnants from the proximal/poste-
nous bone of the mandible; however, it is physi­cally separate from and its development is chronologically later than Meckel’s cartilage. Like other primary cartilages in the human, Meckel’s cartilage is a rod of fetal cartilaginous skeleton in the mandible that begins with conden­sation of the cells to form a precartilaginous blas­tema very early in development (4–5weeks of development) and forms the fetal template or anlagen of the developing mandible. Similar to primary limb cartilage, Meckel’s cartilage arises
rior part of Meckel’s cartilage persist as the malleus and incus, the intermediate/central part of Meckel’s cartilage persists as the anterior ligament of the malleus and the sphenomandibular ligament, while the distal/anterior part of Meckel’s cartilage persists in the mandibular symphy­seal area. (Adapted and redrawn from Fawcett (1924). The
Growth of the Jaws, Normal and Abnormal in Health and Disease)
bones of the middle ear. During the rst 16–18weeks of prenatal life, the synovial joint between the malleus and incus is thought to func­tion as the (primary) jaw joint. Subsequently, portions of Meckel’s cartilage differentiate into various tissues [8]. After it loses its function at 18–20 weeks (as the TMJ begins to function), Meckel’s cartilage is gradually resorbed; in the adult, remnants of Meckel’s cartilage exist as two ear ossicles, malleus and incus, and the spheno­mandibular ligament (Fig.3).
from the mesenchyme of mesodermal origin via interaction with epithelial mesenchyme. This car­tilage is located bilaterally and is positioned lat­eral to the developing mandibular bone but contributes little to mandibular bone formation
2.2 Development oftheCondylar
Cartilage andMandibular Condyle
[8]. This blastema extends as a solid hyaline car­tilaginous rod surrounded by a brocellular cap­sule and extends from the developing ear region to the midline of the fused mandibular processes that forms the tip of the future chin. Along most of its length, Meckel’s cartilage acts as a scaffold, lateral to which the mandible develops via intra­membranous ossication. At its proximal end, Meckel’s cartilage is continuous with the carti­lage, which will form the malleus and incus
Once the mandibular ramus is formed using Meckel’s cartilage as a scaffold, the condylar cartilage begins to develop from the periosteum of the mandibular ramus. A typical periosteum in the adult has two layers—an outer brous layer (protective in function) and an inner osteogenic layer (responsible for differentiation of cells dur­ing intramembranous bone formation). The peri­chondrium of the mandibular condylar cartilage
The Temporomandibular Joint: Form andFunction
7
is continuous with the periosteum of the man­dibular ramus. During development of the con­dylar cartilage, the outer brous layer of the periosteum of the mandibular ramus continues to develop superiorly as the articular layer of the mandibular condylar cartilage (protective in function, and is in contact with the articular disc and the articular eminence of the temporal bone), while the inner osteogenic layer of the perios­teum of the mandibular ramus develops superi­orly to form the pre-chondroblastic layer of the developing mandibular condylar cartilage (responsible for differentiation and source of chondroprogenitor cells during intramembra­nous bone formation) (Fig. 4
). Since the pre-
chondroblastic layer originally develops from
the osteogenic layer of the periosteum, it still retains the ability to differentiate not only into chondroblasts but also into bone-forming cells under the right stimulus, and they are therefore appropriately referred to as “skeletoblast” cells. These two most supercial layers of the condy­lar cartilage (articular and pre-chondroblastic layers) constitute the perichondrial articular envelope (Fig.5). The articular layer is primarily made up of broblasts in a type I collagen matrix with some elastic bers. This layer exhibits very low cell turnover. The pre-chondroblastic layer of the developing condylar cartilage is made up of multipotent mesenchymal cells in a sparse matrix containing type I collagen and proteogly­cans. Immediately below the perichondrial artic-
Fig. 4 Development of condylar cartilage. Alcian blue staining showing the layers in a developing mandibular condylar cartilage (MCC) of a rat. The outer brous layer of the periosteum of the developing mandibular ramus is continuous with and develops into the outer articular layer of the MCC (indicated by the orange arrowheads). The osteogenic layer of the periosteum develops into the pre-
chondroblastic layer of the MCC (indicated by the green arrowheads). The histological image also shows the devel­oping layer of chondroblasts (indicated by the pink arrow­heads). (Image adapted from Hinton, R.J. (2014), Genes
that regulate morphogenesis and growth of the temporo­mandibular joint: A review. Dev. Dyn., 243: 864-874.
https://doi.org/10.1002/dvdy.24130)
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A. R. Joy-Thomas and R. D. Spears
Fig. 5 Histological layers of condylar cartilage. Histological section with Attwood’s staining showing the layers in a developing mandibular condylar cartilage (MCC) of a rat mandible. The layers from superior to infe­rior include an outer articular layer, a pre-chondroblastic
ular envelope (articular layer and pre-chondroblastic layer) is the chondroblastic layer, which is made up of multiple layers of cells. Unlike the layers of chondroblasts seen in the growth plates of long bones or in the cranial base (anisotropic growth), these chondroblasts are not oriented in palisades or rows, but rather have no obvious directional orientation (isotro­pic growth). The chondroblastic layer begins with a zone of attened cells and progresses to more rounded chondroblasts. These cells have considerably more matrix than seen in the pre­chondroblastic layer. The matrix is rich in type II collagen and aggrecan. The next layer of cells in
layer, a chondroblastic layer, a hypertrophic layer, and a zone of mineralization or bone formation. (Image adapted
from Hinton RJ, Jing J, Feng JQ.Genetic Inuences on Temporomandibular Joint Development and Growth.
2015. Curr. Tops. Dev. Biol., Vol. 115, p.85-109)
the developing condylar cartilage is the hyper­trophic layer wherein the cells enlarge greatly and eventually hypertrophy. The matrix contains both type I and type II collagen, with type I col­lagen more prevalent closer to the cartilage- bone interface. Type X collagen, a synthetic product specic to hypertrophic chondrocytes, is also present. The deeper layers show signs of miner­alization as the next layer, i.e., the cartilage-bone interface, is approached (Fig. 5). At the carti­lage-bone interface, blood vessels invade the developing tissue, bringing with them cells that help destroy the cartilage matrix. The hypertro­phic chondrocytes undergo apoptosis or meta-