BMUs can be activated through various stimuli:

Another lesson that Fig. 9.4 holds for our work is that any implant treatment of patients past the age of 35 will be performed on a relatively inactive, resting osteonal system characterized by a very low degree of remodelling per se. The remodelling triggered by the implant procedure will then first induce remodelling of the surgical site, but the processes will extend throughout the entire jaw segments. The main factors determining the direction of this remodelling are force-related effects by macrotrajectories and in the interface area, but also hormonal influences as far as the direction and extent of bone remodelling are concerned. Implant treatments performed on patients under 25 years, by contrast, are not likely to trigger a lot of additional remodelling, so that the effects on macrotrajectories will be smaller as well (see also Marx and Garg 1998). Recently preoperated sites, however, show a higher BMU activation rate due to ongoing remodelling. The placement of BOI implants in these areas is still possible, but immediate loading may not be advisable.

Histological studies are an important element of implantological research. Another notable implication of Fig. 9.4 is that the implantological data obtained in animal experiments cannot be readily translated to humans, since they are usually performed on young adult animals (i.e. shortly after growth has been completed). Those young animals are thus in another “phase of bone life”, corresponding to the leftmost segment of our graph, while our dental implant patients tend to be past 40, thus showing a small degree of spontaneous BMU activity; their osteonal systems are more or less at rest.

The following conclusions can be drawn:

Hyaline cartilage can be neither mineralized nor processed by osteoblasts; they undergo no modelling or remodelling whatsoever. By contrast, remodelling does take place in fibrous cartilage, such as the cartilage covering the TMJs.

This difference appears logical if we consider the following facts:

The age of bone samples of known topographical origin (e.g. from tibial bone) can be accurately determined based on the number of secondary osteons in any given cross-section. On this basis, the age of a patient can be pinpointed to ±5–7 years (Hattner and Frost 1963). Thus the number of secondary osteons gradually rises throughout life; over the years, they become increasingly overlapped and condensed (Kerley 1965). The long tubular bones have a tendency to “straighten out” in accordance with their function over time. ¹ Anyone who has had an opportunity to monitor anatomical developments in the first years of life may have noted that the thighs will straighten out all of a sudden once the child is beginning to walk. In this situation, the strong flexion is not longer acceptable from a mechanical viewpoint, but this problem is solved amazingly fast in accordance with Frost’s flexural neutralization theory (FNT). The crucial mechanism is periosteal modelling along the concave bone segments.

In phases of substantial growth, the rate of bone remodelling is greater in children than in adults, which is naturally due to the hormonal situation. Due to the fast speed of growth in adolescents, the degree of mineralization may sometimes lag behind. The formation of plexiform bone as a temporary corsage is one of the precautions that the live bone may take against fracture as the stresses are continuously changing both in degree and in direction. Because the activity is usually decreased in adults as well, the frequency of BMU activation drops quickly. Apparently, this results in a shortage of activation which is then counteracted by a new rise in frequency.

Contrary to a widespread misconception, jawbones show resorption not because they are subjected to (denture) pressure, but because they suffer from undernourishment combined with a lack of drainage. ² Pressure, as a rule, creates bone.

The observation that the vertical bone volume (particularly in the posterior segment of the mandible) rapidly decreases after insertion of a denture (Blatterfein and Payne 1985) has prompted explanations to the effect that the bone is “pushed away”. This notion of a denture-related pressure atrophy continues to be taught at dental schools and is firmly planted in dentists’ heads, despite the well-known fact that there is no relationship between the surface area of the denture base and the extent of atrophy, although such a relationship would be logical if the pressure per surface unit were a relevant factor (Suenaga et al. 1997).

Consequently, the reduction in bone volume is not due to the chewing pressure but to a combination of individual factors such as lack of intrabony blood supply in the absence of a drainage pathway from the crestal mucosa, which affects periosteal regeneration. Subsequently, the mandibular artery will be more susceptible than most other arteries to sclerosis and partial closure (Bradley 1975). This is particularly true after the teeth have been extracted. This artery is around 15 years ahead of the major carotid artery in terms of its degree of sclerosis. Therefore, the central blood supply to the mandible will be significantly reduced particularly in situations of advanced resorption (Mercier and Vinet 1983). Following tooth loss, the bone-stimulating function along the dental roots is gone, so that the alveolar jaw areas will simply succumb to disuse atrophy. The reason why the blood supply to the mandible is greatly reduced is that no more drainage pathways are present following tooth loss. While teeth are present, the bloodstream to the mandible is distributed to the dental roots and the periodontal ligament – where great amounts of blood are needed on a continuous basis to maintain the local immune system and nourish the tissues – and is drained through the subperiosteal tissue. After the last tooth has been extracted, the bone will close in a definitive manner, and the interior of the mandible becomes congested. The last remaining drainage pathway through the mental artery is overly narrow. Even while teeth are still present, the increase in mineralization in the mandible will significantly raise the resistance to intravasal pressure of the mandibular artery in the 4th decade of life, so that the direction of the blood supply may conceivably be reversed, thus going from the periphery to the centre, in some people. In heavily resorbed mandibles (i.e. in the remaining basal segments) it is known anyway that the bulk of the blood supply is guided from the peripheral zone through the periosteum. In other words, a number of points can be made to support the notion that the pattern of blood supply changes in the wake of bone loss along the alveolar crest. The main purpose of the extensive intrabony blood supply, which is without parallel in the human skeleton, is to nourish the teeth and to fight any infections associated with their presence. Otherwise, the mandibular artery would have to communicate with the “mandibular vein” after the terminal branches and capillaries contained in the teeth and periodontium have been lost.

Against the background outlined above, one of the essential problems with crestal implants in resorbed ridges appears to be that the interior blood supply needed to offer immune defence and enossal force transmission has been almost or completely drained by the time of implant placement. BOI implants, by contrast, mainly require the periosteal blood supply and drainage to be integrated and for force transmission to be supported. This blood supply will be available equally well at any age, even in situations of advanced ridge resorption. More importantly, it can be regulated much better and faster than the intrabony blood supply of the maxilla and mandible.

Any removable restorations inserted in the posterior segment will influence jaw movements by significantly reducing the vertical range of masticatory movements and reducing the lateral excursions in a matter of only around 2 years (Tallgren et al. 1989). These functional alterations will give rise to the qualitative changes in jaw morphology commonly observed in patients wearing dentures. Similar results are seen when the occlusal table on fixed restorations is small.

Conversely, the same functional alterations can give rise to a gain in bone volume after BOI treatment. The reader is referred to Chapter 9.3 for an exhaustive discussion of this mechanism.

Evidence for the existence of a relationship between drainage conditions and bone volume has been provided by Yaffe et al. (1994), who unilaterally mobilized mucoperiosteal flaps in the mandibles of rats, which were then immediately repositioned without suturing after only 30 s. The jaws were histologically followed up by comparing both sides after 3, 7, 10, 21 and 120 days. Massive resorption of the alveolar and endosteal bone was present after only 10 days. The impressive pictures in that report clearly show how much internal damage can be caused by external flap formation if no draining osteotomy is left after closing the flap. Bilateral (i.e. lingual and vestibular) flaps resulted in a greater degree of resorption than unilateral flaps, as the bloodstream is cut off altogether. After 120 days, the alveolar ridges were largely restored. It follows that this atrophy of internal bone structures is due to insufficient drainage, which in turn will cause the incoming blood supply to be reduced as well, thereby causing undernutrition. The open slots following the insertion of BOI implants are presumably capable of preventing this stasis.

During the development of periodontitis, the overpressure generated by the external periodontal tissue appears to obstruct drainage from the interior of the bone, which eventually leads to a deleterious state of stasis. Wang et al. (2003) showed that the average interstitial pressure will be elevated in situations of venous stasis and thus may influence at least the formation of periosteal bone.

In addition to directly influencing bacterial cultures, dental ultrasonic therapy apparently has a mechanical effect on this stasis and helps to restore regular flow conditions particularly in those regions that are not subject to the rhythmical bloodstream – i.e. in the osteonal structures where the internal flow of nutrients and waste products are conveyed by capillary action and mechanical deformation of the bone.. The reason why peri-implantitis therapy often fails may be that the rough surfaces are re-populated by microorganisms already during the healing phase that will immediately enhance the blood supply and cellular granulation, thereby impeding drainage. Compression screws featuring wide windings might therefore be less susceptible to peri-implantitis than solid screw implants, as the flanks of the windings will direct the intrabony bloodstream away from the implant. Moreover, osseointegration is synonymous with vertical corticalization in crestal implant designs. However, since cortical bone structures decelerate the flow of blood and nutrients, periosteal nourishment and periosteal drainage are important, but they are automatically disrupted after surgical treatment of periodontitis with flaps. Around implants, the transport of nutrients is greatly impeded by the implant itself, the blockage depending on their diameter and length. Short implants featuring surfaces that allow internal perfusion (e.g. Osseopore implants) have been successfully employed both in dental implantology and in orthopaedic surgery. These designs overcome the problem of nutrient conveyance by having a permeable surface. The longer these implants, the less likely they will survive, since the perfusion effect is reduced with increasing length, and mineralization in the interface area is reduced as well as bone areas of different macrotrajectorial orientation are crossed by the implant.

As soon as plaque-induced gingivitis results in a swelling of the gums, there is a risk that the flow of blood from the periodontal perfusion space is halted or at least impeded. If this happens, and if the perfusion of the bone is compromised as a result, gingivitis will turn periodontitis, accompanied by a bone reaction (atrophy) caused by reduced perfusion. At the same time, the local pH changes, and immunological competence is decreased.

For the reasons stated above, we regard it as an open question whether bacteria are really causally involved in the progression of periodontitis in the way we are taught to think. Ximenez et al. (2000) showed that the bacterial composition observed in periodontal pockets is also present in the supragingival plaque of patients with healthy periodontium. After all, it would be conceivable that those opportunistic microorganisms may be attracted by the degradation products of the increasingly undernourished periodontal pocket and may advance deeper for different reasons at a later time. In other words, the stasis that will eventually give rise to bone resorption may be caused by a gingivitis-related pressure reversal in the peripheral periodontal vessels. By way of analogy, no observer would assume that the vultures sitting on a dead gnu in the African savannah have actually killed the gnu. Current periodontological thinking does, however, assume that the bone is actually attacked or by the bacteria. Now, while there is no doubt that bacteria will facilitate the progression of periodontal disease, there are numerous indications arguing against their causal role in bone resorption.

It is well known that the anchorage of functional teeth in their bony bed is increasingly lost as periodontal disease progresses. As a consequence, microcirculation is reduced. Loginova and Krechina (1998) showed that microcirculation following the onset of masticatory function (as assessed with chewing gum) increased by 70% in the absence of periodontal disease. In moderate disease, the increase was 19–31%. In cases of severe deep periodontitis, however, the situation was reversed, i.e. circulation would even decrease by 6% (Loginova and Krechina 1998). The authors attributed this finding to changes in vascular micro-architecture involving, among other things, a reversed pressure relationship in the periodontal vessels. In this situation, the crestal segments of the periodontium are supplied from the periosteum and mucosa, while the basal segments continue to be supplied from the enossal space. Under normal pressure conditions, the enossal blood supply would drain to the periosteum and mucosa, but in the specific situation of acute infection, drainage is obstructed by the internal pressure increase in the crestal periodontium. Therefore, periodontitis is essentially a disease in which the bone is depleted of nutrients as the blood flow is undermined by blocking the drainage. The volume of the undernourished bone structures is reduced and it will be replaced by soft-tissue structures. These tissues are susceptible to inflammation caused by the numerous degradation products of the bone in general (enzymes, etc.) and the osteolysis-related high ion levels in particular. The newly formed periodontal tissue structures at the depleted alveolar crest are, in their turn, not particularly well suited to resorb these massive ion concentrations and bone degradation products. In order to ensure drainage of these products, the blood circulation through the crestal periodontium needs to be increased, which becomes clinically manifest as a heightened bleeding tendency.

Some indications to this effect are known to all dentists. Whenever teeth surrounded by large granulomatous regions are extracted, the granulomatous tissue will bleed heavily. The bleeding will stop quickly once the granuloma tissue has been removed. Thus the bleeding originates not in the bone but in the soft tissue. The bone frequently shows large cribriform openings in the contact area with the granuloma without bleeding from these openings when this tissue is removed. The same effect can be observed at childbirth where uterine haemorrhage is stopped quickly after the placenta has been dislodged; if the separation, however, fails or is incomplete, the haemorrhage may persist to the point of becoming life-threatening. Bleeding from the placenta itself is negligible because the lumen of the bloodstream from the newborn organism is too small, which is similar to the blood supply situation in the jawbone; the pressure is thus too low and, more importantly, cannot be regulated upward. In placenta, separate bloodstreams are exchanged at the interface. Jaw granulomas, by comparison, basically stem from one single bloodstream, but the pressure relationships in the area of the terminal branches are such that the pressure coming from the soft tissue prevails. This is the cause of the progressive development unfolding towards the bone, but originating at the soft tissues. The ancient wisdom of bone surgeons, «God protect us from the soft tissues», expresses the recognition that the bone itself is a reliable partner of our implantological work, but that the development and the healing process of the soft tissues are often cause for concern. This is equally true in periodontology, where the displacement of the hard tissues by the proliferating soft tissues is the very essence of the disease. Bone, as a rule, tolerates less nutrition and a lack of oxygen better than too much of both.

The bone is normally unable, for anatomical reasons, to change its internal blood supply. We doubt that bone that is as well-perfused as soft tissue could remain highly mineralized and that it would remain a substance which would be recognized as «bone» at all. It seems likely that overload osteolysis at disk plates occurs due to high perfusion initiated by the healing process after numerous cracks have occurred in the same region of the cortical bone. An accumulation of porosities due to pronounced remodelling may also contribute to the development of cortical defects of this type.

Quite a few questions remain open about the nature of bone at the nano scale. It is clear that the molecular structure of bone is responsible for the strength of the final product (Landis 1995; Huajian et al. 2003). This may imply, however, that the widely used engineering concept of stress concentration at flaw locations may not be applicable at the level of those nanoparticles of which bone consists. The results of the investigations and ideas of Frost presently form a sufficient basis for the implantologist’s work within the jawbones.

From today’s vantage point, it is doubtful that vertically osseointegrated implant surfaces can stimulate the bone sufficiently to ensure that the bone volume is maintained. At least in the collar area, the forces that would cause the bone to remineralize will often be weaker than the forces promoting demineralization as a consequence of bacterial attack. This process gives rise to the crater-style collapses seen with crestal implants. In order to prevent bacterial retention, some crestal implant types come with a hybrid design in which the crestal segments do not feature surface enlargement. These designs have mainly been used for implants with very small threads and without horizontal load-transmitting surfaces. From the fact that these smooth surfaces are not capable of transmitting loads, it follows that even implants featuring vertical load-transmitting surfaces need to undergo basal osseointegration if they are to survive in an environment like the jaw characterized by high bacterial loads.

Although electric potentials are known to be capable of influencing the mechanism and direction of bone healing, it has not been demonstrated that electromagnetic fields applied directly on titanium implants can promote «healing» of the peri-implant bone structures (Buzza et al. 2003).

As BMUs are formed, the bone becomes more porous and thus less resistant. The degree of mineralization in remodelled bone is 20–35% lower than in fully mineralized primary bone structures. The loss in tensile strength is greater than the loss in shear strength. When the elastic range is exceeded, plastic deformation will occur even in osteonal bone, and it will occur earlier in remodelled areas. The attainable level of plastic deformation is highest if the direction of the incoming load is parallel to the osteons. If an equivalent load meets the osteons axially, the attainable level of plastic deformation is smaller.

Osteonal perfusion is caused by the pressure and frequency of blood circulation (10 mm Hg at 2 Hz) and muscle contraction (30 mmHg at 1 Hz); the most important aspect, however, is mechanical loading (100 microstain at 1 Hz). Capillary forces play a role as well (Wang et al. 1999). Permeability across cement lines is, however, irrelevant. An increase of stress cycles per time unit will, however, result in a more pronounced fluid pressure gradient near the osteonal canals.

Bone is a material that is capable of developing a trabecular structure by itself. Bone is also capable of changing the distribution of the load transmission task between different areas inside the bone or within the cortical bone (Mullender et al. 1994). A hypothetical perfectly homogeneous isotropic bone block would become increasingly anisotropic on being subjected to functional loading. In this process, it would develop both areas of heightened and areas of reduced mineralization. This behaviour is known as the «0–1 property». This behaviour is actually quite amazing, as the contact areas of the trabeculae, if for purely mathematical considerations, are always likely to be associated with peak stresses and hence with osteolytic tendencies. This effect, which is known as «checkerboarding», clearly indicates that we are unable to capture the true crux of the matter with our mechanistic thinking and mathematical systems such as FEM models, since all these approaches fail to account for the fuzzy behaviour of live bone. Mechanical testing of bone properties will per se induce bone remodelling, thereby causing the mechanical properties to change.

Will Zurich stop at this train?

(Albert Einstein)

This chapter will certainly be the most interesting part of the book for the knowledgeable reader, as the dental literature does not contain a great many synoptic discussions of the facts herein described. The conclusions drawn from these observations, if applied in a consistent manner, would impact upon the entire field of dentistry and would call into question many aspects of what we have come to regard as best practice in our everyday clinical work into question. The compilation of individual factors in the middle of the chapter will provide the reader with more food for thought but will take a great amount of clinical perceptiveness and technical dexterity to be implemented. The quotation above characterizes the theory of relativity. With regard to the morphological changes caused by dental implantology and subsequent prosthetics, we might want to use a different wording: Where is the real reference point within the jaw bones?

May the quotation above sharpen the reader‘s awareness of the consequences of absolute relativity and of the all-embracing interdependence of all changes in jaws with intact dentitions and in jawbones with implant-supported restorations. Due to the gradual development of morphological changes, dentists and patients are often not aware of their extensive implications. As a result, these changes are not followed up properly, and they are utilized much too rarely for therapeutic purposes.

Our daily work with BOI has taught us to focus our attention primarily on masticatory function, since the role of mastication is much more important than the concept of static occlusion. The differences of BOI compared to conventional prosthetic approaches relying on natural teeth and crestal implants are substantial. For example, the usefulness of reducing the width of implant-supported teeth has never been demonstrated, although the demand has frequently been raised (Mericske-Stern 2000).

In situations where well-anchored teeth with long roots or long crestal implants are available in adequate numbers, the points discussed in this chapter might seem not all that important. After all, long-lasting structures (i.e. structures lasting out the warranty period) can be built on foundations like this even when any masticatory considerations are completely ignored. Nevertheless, any screw fractures, porcelain chipping, periodontal tooth mobility and/or implants lost will indicate that forces are present that are not tolerated well or that biomechanical developments do not seem to unfold according to plan.

Anyway, the BOI implantologist rarely gets to work under such favourable conditions but is usually faced by advanced vertical ridge resorption allowing only extremely small force-transmitting areas to be inserted into the bone. Therefore, any excessive prosthetic loading needs to be avoided or eliminated. On the other hand, BOI implants will allow some freedom with regard to the length and nature of the chewing surfaces.

In addition, the effects of the masticatory function on bone morphology need to be considered as well.

The following list provides some food for thought: