Bone is a mineralized connective tissue. Approximately 60% of the wet weight of bone is inorganic mineral, with 25% organic matrix and the remaining 15% water. The mineral phase provides the hardness and rigidity of bone and consists of carbonated hydroxyapatite, present in the form of thin needle-like crystallites or thin plates (about 50 nm wide, up to 8 nm thick and of variable length) distributed between the gap zones of the collagen molecules. The organic matrix contributes to other aspects of its physical properties, such as tensile strength and modulus of elasticity, and is approximately 90% type I collagen. Most collagen can be regarded as intrinsic collagen secreted by osteoblasts. However, collagen inserted as Sharpey fibres from the periodontal ligament can be considered as extrinsic collagen. The non-collagenous matrix is a heterogenous group of proteins, which accounts for 10% of the organic matrix. These proteins include the proteoglycans, which incorporate chondroitin and heparan sulphate glycosaminoglycans, mainly in the form of decorin and biglycan. Glycoproteins associated with bone include osteopontin, osteonectin, bone sialoprotein (BSP), osteocalcin and fibronectin. The part played by these individual proteoglycans still requires clarification; however, they may have important roles in bone formation and subsequent mineralization. Bone also contains exogenously derived proteins that may circulate in the blood. These include albumin and also a varied cocktail of cytokines and growth factors, including interleukins, tumour necrosis factor, TGF-β, FGF, PDGF and BMPs. These bioactive molecules are stored or locked up within the bone matrix. Release of these molecules during trauma or general remodelling may play a role in controlling further bone activity.

There are a number of ways that the classification of bone can be achieved:

The alveolar, tooth-bearing portion of the jaws is composed of outer and inner alveolar plates. The individual sockets are separated by plates of bone termed the interdental septa, while the roots of multirooted teeth are divided by inter-radicular septa. The compact layer of bone lining the tooth socket has been referred to as the cribriform plate, reflecting the sieve-like appearance produced by the numerous vascular canals (Volkmann’s canals) passing between the alveolar bone and the periodontal ligament. It has also been called bundle bone because numerous bundles of Sharpey fibres pass into it from the periodontal ligament. In clinical radiographs, the bone lining the alveolus commonly appears as a dense white line and is given the name lamina dura. Between the bundle bone and the inner and outer plates of compact bone are variable amounts of spongy bone, depending on site.

Bone is deposited in layers, or lamellae, each being 3–5 μm thick.

Bone contains several different cell types that are responsible for the synthesis, maintenance and resorption of bone. They can be regarded as belonging to two main families, one mesenchymal and the other haemopoietic:

Extrinsic Sharpey fibres inserting into the cribriform plate are derived from the principal fibres of the periodontal ligament. Sharpey fibres are particularly prominent in the cervical portion (alveolar crest region) of the alveolar bone. Here, where bone is compact, Sharpey fibres may penetrate the bone to a considerable depth. Sharpey fibres entering alveolar bone are less numerous but thicker than those at the cementum surface. Because of the attachments of numerous bundles of collagen fibres, the cribriform plate has also been called bundle bone.

Structural lines are evident in bone. Bone is laid down rhythmically, which results in the formation of regular parallel lines that, because they are formed in periods of relative quiescence, are termed resting lines. Such resting lines differ biochemically from adjacent bone. These lines are prominent in bundle bone on the distal surface of the socket wall during physiological mesial drift of the teeth. Bone will also contain reversal lines, representing the site of change from bone resorption to bone deposition. Such reversal lines will show evidence of a scalloped outline, reflecting the position of Howship’s lacunae.

There is close correlation between resorption and deposition of bone. The osteoclast has far fewer surface receptors than the osteoblast and is not directly responsive to the majority of hormones or growth factors. This has led to the concept that the osteoblast has a controlling influence in the development and maturation of the osteoclast. However, important receptors that the osteoclast does express are those for calcitonin (a powerful inhibitor of osteoclasis that interferes with the cell attachment mechanism to bone), prostaglandins and RANK (receptor activator of nuclear factor kappa B).

The processes of bone resorption and formation at sites of remodelling do not occur randomly. Clearly, there must be tight control to ensure a balance between the two processes, as any disruption of this balance can lead to metabolic bone disease (such as osteopetrosis and osteoporosis). This close control can be referred to as coupling. From a resting state, the sequence of remodelling consists of four main phases:

There is thus a clear relationship between bone deposition and bone resorption, and this relationship is mediated biochemically. Many of the factors that result in bone resorption do not have direct effects on osteoclasts but act through osteoblasts, as most receptors to the bioactive molecules responsible for resorption are present on the osteoblast. How the osteoblast promotes resorption may be through the release of bioactive proteins such as cytokines and growth factors, including macrophage colony stimulating factor (MSC-F), osteoprotegerin, receptor activator of nuclear factor kappa B ligand (RANKL), and interleukins, which may stimulate the production of osteoclasts. Osteoblasts may release MMPs, degrading the osteoid on the bone surface, exposing the mineralized bone matrix, and allowing osteoclasts to attach themselves to the mineralized bone and begin resorption. Whilst the precise signals responsible for causing the cessation of resorption and a reversal to osteoblast differentiation and activation of bone formation are not known, the release of molecules such as growth factors, initially bound up in the bone matrix but exposed/activated by the resorption process, may be involved. For example, BMPs and IGF released from bone may stimulate osteoblastogenesis, while TGF-β released from bone may inhibit osteoclastogenesis while stimulating osteoblastogenesis. These bone-bound bioactive growth factors are activated by subsequent osteoclastic bone resorption and bind to their receptors on osteoblasts and osteoclasts, influencing bone remodelling. Ambient pH and levels of oxygen are also important factors affecting resorption.

As a reduction in the mechanical loads impinging on bone is associated with bone loss, it can be assumed that such loading is normally required to stimulate the modelling/remodelling processes of bone necessary to maintain normal bone structure. Strains need to be intermittent (rather than continuous), and the osteogenic response is dependent upon the size of the load and the frequency and rate of application. To maintain bone mass may only require the application of relatively few loading cycles.

The molecular mechanisms whereby forces impinging on the bone are transduced into bone resorption or deposition remain elusive, although many theories have been proposed. Osteocytes, together with the surface layer of osteoblasts/bone-lining cells, appear to be the most obvious candidates for detecting strain within bone. Deformation of bone following loading is thought to deform the cell processes/cell membranes either directly, or indirectly through movement of tissue fluid residing in the lacuno-canalicular system. Signals are then transduced via the cell membrane at the surface (e.g. involving K ⁺ and Ca ²⁺ ion channels and integrins) to cytoskeletal elements within the cell, with stimulation of secondary messengers. These changes eventually lead to the production and release of molecules that initiate an osteogenic response.