W. Eugene Roberts and Clark M. Stanford

Chapter Outline

Osteology of the Maxilla and Mandible

To understand the outcomes of implant therapy, the dental practitioner must understand the bone morphology (osteology) of the craniofacial complex. A frontal section of an adult skull shows the bilateral symmetry of bone morphology and functional loading (Figures 4-2 and 4-3). As shown in Figure 4-3, the vertical components of the cranium tend to be loaded in compression (conveyed as a negative stress, by convention in engineering), and the horizontal components are loaded in tension (positive stress). This is one of the most efficient structures for achieving maximal compressive strength with minimal mass in a composite material.

As Figure 4-3 shows, no net tension exists across the palate in an adult. During the prenatal and early postnatal period, the palate grows in width through the posterior palatal synchondosis (primary growth center).¹ This is one important reason implant placement should be delayed until skeletal maturity has been reached. Otherwise, an implant becomes positioned too far from the palatal aspect of the occlusal plane.

Although equal and opposite functional loads are delivered to the maxilla and mandible, the maxilla transfers stress to the entire cranium, whereas the mandible absorbs the entire load. Consequently, the mandible is stiffer than the maxilla. A midsagittal section through the incisors (Figure 4-4) and a frontal section through the molar region (Figure 4-5) show the distinct differences in the osseous morphology of the maxilla and mandible. This should be carefully evaluated with regard to implant placement, because the type of bone contact and proximity to the cortical plates influence when the implants can be safely loaded.

The maxilla has relatively thin cortices interconnected by a network of trabeculae (see Figures 4-2, 4-4, and 4-5). Because it is loaded primarily in compression, the maxilla is structurally similar to the body of a vertebra. The mandible, however, has thick cortices with radially oriented trabeculae (Figures 4-4 and 4-5). The structural array is similar to that for the shaft of a long bone, indicating that the mandible is loaded predominantly in bending and torsion. For this reason, mandibular flexure often influences implant prosthesis design. This biomechanical impression based on osteology is confirmed by in vivo strain gauge studies in monkeys. Hylander^2,3 demonstrated substantial bending and torsion in the body of the mandible associated with normal masticatory function (Figure 4-6). This is an important issue in implant treatment planning, because implant prostheses that cross the mandibular midline or extend into the molar area undergo torsional stress. This mechanical overload can lead to prosthesis fracture, material failure, and possibly implant or implant abutment fracture.

Bone Physiology

The physiology of bone has proven elusive for investigators because of the technical limitations inherent in the study of mineralized tissues. Accurate assessment of the response of bone to mastication requires time markers (bone labels) and physiologic indexes (e.g., deoxyribonucleic acid [DNA] labels, histochemistry, and in situ hybridization) of bone cell function. Systematic investigation with these advanced methods has defined new concepts of clinically relevant bone physiology, such as mineralized sectioning, birefringence analysis, fluorescent labeling (often with tetracycline-based markers to determine rates of bone growth), microradiography, cell morphology measurements, finite elemental modeling of bone stress and strain, and electron microscopy to evaluate bone density and microarchitecture.4–19

Bone Tissue Responses to Dental Implant Placement

After implant placement, relatively immature new bone forms rapidly at the implant interface; this bone is later replaced by a more complex but stronger bone along the interface. In general, there are four types of bone established during normal healing and remodeling phases: woven bone, lamellar bone, composite bone, and bundle bone.

Skeletal Adaptation: Modeling and Remodeling

Skeletal adaptation to the mechanical environment is achieved through changes in (1) bone mass, (2) geometric distribution, (3) matrix organization, and (4) collagen orientation of the lamellae. In addition to these adaptive mechanisms, which influence bone formation, the mechanical properties of osseous structures change as a result of maturation, function, aging, and pathologic processes. Examples of physiologic and pathologic factors include secondary mineralization, mean bone age, fatigue damage, and loss of vitality (pathologic hypermineralization).²⁸

Trabecular bone and cortical bone grow, adapt, and turn over by means of two fundamentally distinct mechanisms, modeling and remodeling. In bone modeling, independent sites of resorption and formation change the form of a bone (i.e., net shape or size, or both). In bone remodeling, a specific coupled sequence of resorption and formation replaces previously existing bone without a net change in size or shape. The mechanism for internal remodeling (turnover) of dense compact bone involves axially oriented cutting and filling cones composed of a coordinated set of osteoclasts and osteoblasts (Figure 4-9).⁴ In implant healing the initial modeling process, which is driven by inflammatory mediators, establishes the implant-bone interface.³⁰ Later, ongoing remodeling mobilizes and deposits calcium apatite mineral by means of coupled resorption and formation: bone is resorbed and deposited at the same site.

Osteocytes, osteoblasts, osteoclasts, and possibly their precursors are thought to communicate by a complex set of growth factors.³¹ Transforming growth factor beta, released from bone during the resorption process, helps to stimulate subsequent bone formation to fill resorption cavities.³² Currently, growth factors released from bone are thought to mediate the coupling process through a genetic mechanism for activating and suppressing osteoclasts (RANK, RANKL, and OPG are gene products that assist in the control of remodeling). This genetic mechanism appears to be involved in the inflammatory induction of bone resorption and the coupling of bone formation at the same site (Figure 4-10).^33,34