From a Crest to a Trough – Understanding Marginal Crestal Bone Loss around Implants.

Chethan Hegde (M.D.S.), Manoj Shetty ( M.D.S.), Krishna D. Prasad ( M.D.S.), Lobo Nikhil Jason ( B.D.S.)

Department of Prosthodontics Including Crown and Bridge and Implantology, A. B. Shetty Memorial Institute of Dental Sciences, Mangalore, India

Abstract:
The preservation of the crestal bone assumes extreme importance with respect to the success of the implant both functionally and esthetically. Various concepts and theories regarding the causes for crestal bone resorption have been prosposed.

The purpose of this article is to evaluate the concepts regarding crestal bone loss and thus enable a better understanding of the phenomenon as well as the inadequacies of individual concepts in explaining its occurrence. The article also highlights the changes which have taken place in the field of implantology in an attempt to preserve the crestal bone.

Introduction:

Dental implants have become a very important part of the prosthodontic treatment of the edentulous patient. Implants have definite advantages over conventional prosthodontic approaches. Success rates for dental implants although high have been found to vary depending upon the implant design and systems being used. ^[1]

Osseointegration was originally defined as a direct structural and functional connection between ordered living bone and the surface of a load-carrying implant. The bone surrounding the implant thus has an inseparable role in implant success. A common method utilized to gauge implant prognosis is the evaluation of the bone levels surrounding the implant .^[2]

Crestal bone loss has commonly been found around implants. Its occurrence can compromise the esthetic result of implants and its progression can eventually lead to failure of the implants.^[3]

Branemark, a pioneer in the field of Implantology, advocated the use of an extensive surgical flap to allow greater access to implant site following which implants were placed and flaps were sutured to allow the site to heal and the implants to osseointegrate. Since then various alterations in flap designs have evolved to involve techniques that claim to preserve bone and result in greater esthetic outcome following implant placement. Long term data comparing the surgical techniques is lacking and thus the true value of these claims cannot be verified. However recent studies seem to indicate comparable values for bone loss following placement by any surgical technique. ^[4]

Acknowledging the phenomenon of crestal bone loss following implant placement and understanding its cause and effect is essential to ensure that our diagnosis and treatment planning aims at minimizing it and ensuring greater implant success and esthetics.

An analysis of the literature reveals that the first study quantifying the amount of crestal bone loss was by Adell et al ^[5] (1981) based upon a 15 year study of osseointegrated implants. He observed an average of 1.2 mm marginal bone loss from the first thread immediately and during the first year after loading. Subsequent years demonstrated bone loss occurred at an average of only 0.1 mm annually

More recent studies report an average first year bone loss of varying values of 0.5mm to 0.93 mm in the 1st year and a mean loss of 0.1 mm thereafter ^[6].
Hence although the amount of crestal bone loss observed may vary, its occurrence is inevitable following implant placement.^[4] Numerous studies have thus identified the phenomenon of marginal crestal bone loss in relation to implants however the exact etiology seems to be unclear and various hypotheses have been put forward which attempt to explain the occurrence of crestal bone resorption.

Reflection of the Periosteal Flap –

Periosteal reflection has been suggested as a cause for crestal bone resorption .

Surgical procedures during implant placement require elevation of a mucoperiosteal flap which causes transitional changes in the blood supply to the crestal bone

When the periosteum is reflected the cortical blood supply is affected and osteoblasts death on the surface of the bone occurs. The blood supply is re-established when regeneration of the periosteum occurs. Apart from the periosteum the crestal bone is also supplied by the underlying trabecular bone/ cancellous bone. Thus in spite of periosteal reflection vascular supply is obtained to some degree from the trabercular bone ^[7]. It is observed that greater the trabercular bone under the crestal bone, the less crestal bone is seen to resorb.

In a study by Jeong et al ^[8], it was observed when implants were placed without elevating a flap, both the amount of osseointegration and the bone height around the implants were greater than in implants placed with surgical procedures involving conventional flap elevation. The mean peri-implant bone height was found to be greater at flapless sites than at sites with flaps . This enhancement is probably due to the preservation of bone vasculature by surgical techniques that alter bone blood supply to a lesser degree.

In sync with this hypothesis Becker et al ^[9] observed that flapless surgery using a minimally invasive technique causes minimal changes in crestal bone levels around implants

Hence reflecting the periosteal flap seems at initial observation to be a plausible explanation for bone loss occurring at surgical sites, however a further evaluation of the type of bone loss seen at implant sites reveals shortcomings of the hypothesis.

Wilderman et al ^[7] found that the horizontal bone loss occurring after osseous surgery involving reflection of the periosteum is approximately 0.8 mm, and ability of the bone to repair is highly dependent upon the amount of cancellous bone present underneath the cortical bone at the site .

Bone loss occurring at stage II implant surgery even in successfully osseointegrated implants is generally of a distinct horizontal saucerisatiom pattern and not of a vertical nature as observed by Wilderman in natural teeth following osseous surgery. The surrounding bone does not seem to show involvement even though reflection of the flap alters its blood supply.

Therefore, this hypothesis although providing important details of bone healing at implant sites, cannot be identified as the sole cause for marginal crestal bone resorption observed at these sites.

Surgical Trauma to the bone / Implant Osteotomy –

Implant placement essentially involves removal of a portion of the bone corresponding to the size of the implant to be placed to allow insertion of the implant body into the bone and enable a close approximation of the implant to bone followed by subsequent osseointergration.

Trauma to the bone during osteotomy procedures that occurs as a result of heat generation or pressure at the crestal region, may be a cause of creation of a devitalized bone zone around the implant. This devitalized bone must be replaced and remodeled by new bone to permit implant osseointegration.

Eriksson and Albrektsson^[10] showed that heating test implants above a temperature of 47°C in 1 minute resulted in reduction of the bone formation at the site. The results of this study demonstrated the importance of controlling temperatures during osteotomy procedures.

Hence the phenomenon of crestal bone resorption can be explained following surgical trauma on account of the weak ability to transmit heat from the crestal region due to its limited blood supply.

The second concept in favor of surgical trauma as a cause of crestal bone resorption is based upon the quality of the crestal bone.

The crestal bone has greater susceptiblty to bone loss due to more dense nature as compared to the underlying trabercular bone. the nature of the crestal bone causes greater heat production at the site and thus bone resorption results .

In support of this concept, Flanagan^[11] observed greater heat production during implant placement in dense bone and thus irrigation must be provided to control the heat generation at sites with dense bone.

Hence although surgical trauma seems to be a suitable explanation, literature with regard to bone density affecting crestal bone resorption revealed no significant relation of crestal bone resorption to the quality of bone at the implant sites.

In a 5 year prospective study by Misch et al ^[12] and another study by Park, they found no statistical differences in crestal bone loss around implants placed in different bone densities ^[3]

If the belief that surgical trauma is the sole cause of crestal bone resortion must be accepted, bone loss should occur immediately following implant osteotomy procedures, that is during the initial healing period and be evident at second stage uncovery. However it is often observed that the bone loss seen at implant sites is not visible at the second stage uncovery of the implants 4 to 8 months later.

Hence surgical trauma as a cause of crestal bone resorption although insightful is unlikely to be the cause of early crestal bone loss.

Host Response to Bacteria and their toxic products -

In a healthy state the host defense mechanisms are able to cope with the damaging metabolites produced by bacteria. If the nature of the flora changes either due to an increase in organisms or their conversion to more virulent strains , host defences may be unable to cope and periodontal destruction occurs.

Periodontal disease and accompanying bone loss around natural teeth is caused by bacteria and their toxic products .The accompanying bone loss is generally of a horizontal or vertical pattern depending on the nature of the causative organisms and host defence mechanisms. ^[13]

The soft tissues adjacent to an osseointegrated implant include connective tissue and epithelium which bear a close similarity to the natural teeth. The tissues although similar to natural teeth possess certain important differences when closely compared. For instance, due to the absence of cementum the fibres in the supracrestal region are oriented parallel to the implant surface in contrast to their orientation in natural teeth . ^[14]

Soft tissue response to plaque has been observed to occur in a similar manner around natural teeth and dental implants. However, with increasing duration of plaque accumulation, the peri-implant mucosa seems to be less effective in encapsulating the inflammatory lesion ^[15]

Hence bacteria may be a definite etiological factor in crestal bone loss around implants.

However in studies by Quirynen et al^[16], they found that the loss in marginal bone height did not clearly correlate with parameters such as the plaque index, the gingivitis index.

Similarly, studies by Adellet al^[5] observed that the microbiotia found surrounding implants comprised coccoid cells and non-motile rods indicating a favorable composition if similar findings had been observed at teeth. They concluded that the prognosis for osseointegrated implants appears excellent, especially with regard to the microbiotia.

Hence although bacteria may have a role in progression of peri-implantitis and eventual implant failure, with regard to crestal bone loss it fails to be identified as the sole causative factor.

To further downplay the role of bacteria is the observation that marginal crestal bone loss occurs maximum in the first year (1.5mm) and shows a decrease (0.1mm) in subsequent years .

An obvious conclusion should be that as the sulcus depth increases at implant sites in subsequent years there should be a shift in the environment to favour a more anaerobic bacteria similar to that seen in the natural dentition and hence more bone loss should be observed. ^[13]

However studies show that gingivitis and increased pocket depths were not associated with signs of increased marginal bone loss around implants. ^[17]

Hence the role of bacteria as primary causal factor inadequately explains the marginal crestal bone loss occurring at implant sites.

Invasion of the Biological Width-

The biological width is the dimension of the soft tissue, which is attached to the portion of the tooth coronal to the crest of the alveolar bone.
This term was based on the work of Gargiulo et al ^[18] 1961), who described the dimensions and demonstrated a definite relationship between the alveolar crest, the connective tissue attachment, the epithelial attachment, and the sulcus depth.

They reported mean dimensions of sulcus depth - 0.69mm, epithelial attachment of 0.97mm, and connective tissue attachment of 1.07mm. The biologic width is commonly valued at 2.04mm, which represents the sum of the epithelial and connective tissue components. ^[18]

It is generally accepted that invasion of the biological width in natural teeth results in gingival inflammation and bone resorption until the biological width is re-established.

The structure of peri-implant mucosa has many similarities with periodontal tissues. The soft tissue barrier is composed of a sulcus with a non keratinized sulcular epithelium, a junctional epithelium, and a supracrestal connective tissue with an area of dense circular fibers adjacent to the implant surface.

The dimension the soft tissue barrier around the implant seems to be constant, similar to what has been described around natural teeth. This dimension has been described as “peri-implant biologic width”:

Tarnow^[19] found because implants available have flat platforms which are being positioned below the inter-implant bone crest the biologic width exists subcrestally. This differs from the natural tooth wherein the biologic width is supracrestal

Most studies report bigger values for peri-implant biologic width than the ones reported for periodontal biologic width. The difference is generally related to a bigger epithelial component at implant sites when compared to the tooth. A minimum dimension of the biological width is needed in order to accommodate for the soft tissue healing process, when this dimension is not present bone resorption may occur, to allow for an “appropriate biological dimension” of the peri-implant soft tissue barrier. ^[20]

However a closer look at the peri-implant soft tissue reveals that although a biological seal is found around implants there appears to be no junctional epithelium component similar to that found around natural teeth. Hence since no connective tissue components are attached to the implant the remodeling of bone to allow formation of a biological width cannot be explained.

None the less the biological width theory explains the bone loss from the stage of first surgery and early bone loss seen in the first year after second stage abutment placement. Hence early crestal bone loss can be identified to result as a mechanism of establishment of the Biologic Width /Seal.

Effect of Microgap-

Two stage implant systems essentially are composed of an implant body and a cover screw or abutment.The gap between the cover screw and the implant body is called ‘Microgap’. The microgap is similar to the crevice between the abutment and the implant body.

Ideal dimension of the microgap should be 0µ as there should be direct metal to metal connection of the components. However in reality dimensions larger than this are often encountered.

The micro-gap is not a cleansable location to patient or professional care, and thus an environment favourable to bacterial growth may exist. For instance loosening of the abutment on the implant placed in a submerged approach causes inflammation, this is due to increase in the microgap favoring bacterial accumulation, tightening of the abutment (reduction of the microgap) is seen to eliminate the infection.

Hermann et al ^[21] were the first to demonstrate that the microgap existing between the implant/abutment has a direct effect on crestal bone loss. Through their radiographic study they observed that the location of the microgap in relation to the alveolar crest whether placed in a submerged or non-submerged approach had a profound influence on alveolar bone surrounding the implants. They also found that submerged implants lose approximately 1.5mm of bone over the first year of function . Earlier studies attributed this to countersinking procedures and stress to which the bone is exposed , however since in their study no restorations were placed, Hermann et al concluded that bone loss occurring was a result of the microgap and creation of the biological width.

If the microgap is exposed to the oral environment greater bone loss is observed. This was demonstrated in a study Barboza et al ^[22]

Broginni et al ^[23] found an intense inflammatory cell infiltrate and significant bone loss associated with the presence of microgap at the bone crest regardless of the surgical technique. They also found greater bone loss around two piece implants as compared to one piece implants

Hence crestal bone resorption as a result of the microgap cannot be ignored. However data does not seem to suggest its role as the sole causative factor of crestal bone resorption.

Bone growth is often observed over the coverscrew during initial healing .Since the microgap existing between the coverscrew and implant body is similar to that between the body and abutment the phenomenon of bone formation in one case and bone resorption in another cannot be completely explained.

Another factor of consideration is how much of the bone loss occurring is related to the surgical procedure of placement of implant abutment connection below the bone level. The bone loss to the first thread observation implies that bone loss occurs until the first thread of the implant is reached . This observation is not consistent with the concept of the reestablishment of biological width nor the presence of implant microgap.

Bone Response to Occlusal load –

Occlusal trauma has been defined as 'injury to the periodontium resulting from occlusal forces which exceed the reparative capacity of the attachment apparatus'. Occlusal trauma may cause bone loss around the implant. However, the determination of the etiology of this bone loss remains controversial.

According to bone physiology theories, bones subjected to mechanical loads adapt their strength to the load applied on it by bone remodeling. This also applies to bone surrounding an oral implant. The bone responds to an increased mechanical stress below a certain threshold by increasing the bone density by apposition. Similarly, bone resorption may be the result of mechanical stress beyond this threshold. ^[24]

The topic of the relationship of marginal bone loss due to occlusal forces is controversial.

Jung YC^[25] conducted a study to determine radiographically the bone loss around implants following implant abutment connection. It was concluded that most of the implants showed resorption of alveolar bone beyond the polished neck at 12 months. The bone level stabilized at the first thread of the implants with no correlation to either the time of exposure of the polished neck or the type of implant. Bone density was seen to decrease at the marginal bone and increase at the newly formed alveolar crest.

Whereas in a review by Vidyasagar and Apse^[26] it was concluded that under excessive loads, bone loss has been demonstrated in some animal studies. In human studies, where overload can be assumed to occur through parafunctional activity, bone loss from overload could not be demonstrated clearly. Bone gain over long term function has been reported by studies, which suggests that functional loading over a certain physiologic range induces a positive bone response.

To better understand the relationship of marginal bone loss to occlusal overload individual aspects of bone and implants must be evaluated.

Strain occurring in a body is described as the change in length of the body per unit original length of the body.

Bone remodeling occurs at the cellular level controlled by varying degrees of strain. The strain induced in the bone surrounding an implant is known to be related to the stress on the implant prosthesis.

In a numerical study by Chainchanasiri et al^[27], it was demonstrated that premature contact in implant restorations leads to high magnitudes of strain in the marginal bone. The area of high strain correlates with the marginal bone loss observed in patients .

An important theory in favor of the role of cellular biomechanics as a cause of crestal bone resorption is Frost‘s Mechanostat Theory.

Frost proposed that bone responds to a complex interaction of strain magnitude and time.
Conceptually the interfacial bone maturation, crestal bone loss and loading can be explained by this theory which connects the two processes of modeling (new bone formation) and remodeling (continuous turnover of older bone without a net change in shape or size). The bone acts like a ‘mechanostat’, in that it brings about a biomechanical adaptation, corresponding to the external conditions.

Frost observed four micro-strain zones and related each zone to mechanical adaptation occurring in the bone .The four zones include the disuse atrophy, steady state, physiologic overload and pathologic overload zones. Both extreme zones (pathologic overload zone and disuse atrophy zone) are proposed to result in a decrease in bone volume. When peak strain magnitude falls below 50-200 µ-strain, disuse atrophy is proposed to occur, a phenomenon that is likely to explain ridge resorption after tooth loss.
In the pathologic overload zone, strain in magnitude of over 4000 µ-strain may result in net bone resorption. [26]
Hence the belief that occlusal forces beyond a certain amount can result in bone resorption is well explained by cellular factors within the bone that respond to the conditions to which the bone is subjected. However to date the extension of bone cellular studies have not been replicated in the bone surrounding an implant.

Another concept based on engineering principles concludes that difference in the modulus of elasticity between implant and bone causes increased stress contours at the bone implant interface. Finite element analysis studies conclude that marginal bone loss follows a similar pattern as the stress contour patterns formed in bone ^[28]

The quality and quantity of bone surrounding the implant is also know to influence the load transfer from implant to the jaw bone. With the correct stress level within the jawbone, the correct amount of stress shielding will occur. Stress shielding is the mechanism that protects the jawbone from stresses that it might encounter by increasing the bone density. Wolff observed that bone is reshaped in response to the forces acting on it and this is referred to as Wolff's law. ^[29]
In a radiographic study by Manz ^[30] he concluded that bone loss was greater in bone having lower quality. Marginal bone loss is less in the mandible compared to the maxilla. The cause maybe the more dense quality of bone encountered in the mandible.

Another factor influencing crestal bone resorption is believed to be cantilever length .

The prognosis of cantilevered fixed partial denture on natural teeth abutments is considered to be poor since its failure rate has been reported 36-40% in a period of 5 to 7 years. The cantilever design has a significant influence on stress distribution in implants and its supporting tissues and can lead to unfavorable biomechanical effects around them .Furthermore, finite element studies revealed that higher stress concentrations developed in models with cantilever prostheses . Therefore, in a long term period, greater marginal bone loss would result and this would jeopardize the health of soft and hard tissues supporting implants ^[31]

In a review of literature by Jose et al^[32] it was concluded that the literature suggests that the incorporation of cantilevers into implant-borne prostheses did not have any significant effect on the amount of peri-implant marginal bone loss, either at the prosthesis level or at the implant next to the cantilever.
Halg et al^[33] it concluded that cantilever on fixed dental prosthesis did not lead to a higher implant failure rate and did not lead to more bone loss around supporting implants compared with implants supporting conventional fixed dental prosthesis.

Therefore while stress on the bone may increase in cantilever designs the effect of cantilevers as a cause of marginal bone loss is still unclear. Hence although the concept of bone response to occlusal loads may be a possible explanation for the causes of crestal bone resorption during the life of the implant. Bone loss from occlusal overload is considered to be more of a progressive phenomenon similar to that occurring in natural teeth rather than limited to the first year of loading.

Biomechanics of Implant design / Crest Module-

It has been suggested that the implant neck should be smooth/ polished, supporting the belief that the crest module should not be designed for load bearing. This is based on the concept that the implant design may affect the magnitude of forces applied at the bone implant interface.

The design of the crest module in addition to magnitude can also effect the type of forces to which the bone is subjected.

Implants with a smooth collar are believed to transmit shear forces to the bone whereas bone is known to be strongest under compressive forces. Under conditions of loading due to shear nature of the forces exerted onto the bone, bone resorption may occur in smooth collar implants until the first thread is reached where the force changes from a shear to a compressive nature. Hence this is cited as the cause of the first thread observation.

Hermann et al^[21] found that titanium implants with rough surface are more osteophilic than implants with a smoother surface. Thus more pronounced bone loss observed is most likely caused by the difference in implant surfaces.

Emanuel et al ^[34]observed that implants with a roughened neck surface and microthreads are more resistant to marginal bone loss during the first phases of healing, as compared with implants with a polished neck.

Piao et al ^[35] evaluated the effect of surface macro-and microstructures within the implant to marginal bone change after loading. They concluded that a rough surface with microthreads at the coronal part of implant, maintained the marginal bone level against functional loading better than implants without these two features.

Similarly a study by Pillar et al^[36] highlighted the importance of implant design in bone remodeling by studying implants having different collar designs
Hence bone resorption as a result of changes in stress levels to which bone is subjected during loading as a result of implant design further adds light to the observations at the crestal bone seen at implant sites.

Platform switching concept as a means to reduce crestal bone loss-

This concept consists of utilizing prosthetic components that are undersized in relation to the diameter of the implant collar in order to limit peri-implant bone resorption.

This strategy arose from observation as early as 1991, of situations in which bone resorption did not occur/occurred minimally around wide 5 mm implants. Crestal bone level were found to remain constant for the entire length of the implant, up to the collar, regardless of the loading period.

This observation was in response to the scenario of major peri-implant bone loss (noticed to occur irreversibly when all two-piece implants were exposed to the oral conditions). Platform switching essentially involves creating a discrepancy between the diameter of the implant platform and the diameter of the prosthetic abutment. This is achieved by using implants with a 5-mm platform and undersized abutments (4.1 mm). A horizontal distance of 0.45 mm is thus created between the implant-abutment interface and the peri-implant tissues.

Implant configuration of this type on being exposed to the oral environment displays the normal reaction. That is the contacting surfaces between implant and abutment undergo colonization by gram-negative and anaerobic bacteria, and a band of connective tissue is generated with large amounts of inflammatory infiltrate around it. However these toxic metabolites are kept away from the implant-abutment interface and also away from the peri-implant bone. This leads to lessening the extent to which colonization of the biologic width occurs and significant reduction in bone loss

In a review of literature by Mari et al^[37], they concluded that the literature suggests that platform switching has the capability of reducton or elimination of crestal bone loss by approximately 1.56 mm ± 0.7 mm. It also contributes to maintenance of the width and height of crestal bone and limits the circumferential bone loss. They went on to conclude that implant design modifications involved in platform switching offer multiple advantages in cases where a larger implant diameter is desirable but space constraints are present with regard to the prosthesis.

In a study by Nebot et al^[38] they found that a significant reduction in bone loss was noticed in cases where the platform geometry was modified as opposed to those for which matching-diameter implant abutments and platforms were used

Hence the literature suggests that alteration in the implant design by platform switching is an effective method of reducing marginal crestal bone loss surrounding implants

Soft Tissue thickness and its relation to crestal bone resorption-

The tissue biotype present influences the esthetic result of the implant due to its relation to crestal bone resorption .

In a prospective study by Linkevicius et al ^[39] it was found that crestal bone stability occurred only at sites with thick tissue. Thin tissue was associated with greater crestal bone loss on account of biologic width formation. Supracrestal placement of implants should be avoided if a thin mucosal biotype is present at the implant site. They also recommend thickening of the mucosa if thin prior to implant placement. In a subsequent publication they noted that that implants with platform switching did not preserve crestal bone better in comparison with implants with traditional implant-abutment connection if, at the time of implant placement, thin mucosal tissues were present.^[40] .

A thick tissue biotype is considered to be a desirable characteristic that will positively affect the esthetic outcome of an implant supported restoration because of the greater resistance of thicker tissue to insult and injury.^[41]

Conclusion :

The primary objective of dental implants is to act as an abutment for a prosthetic device closely reproducing a natural tooth. However fundamental differences in the support between the implant and natural tooth must be recognized. Various theories attempt to explain the causes of crestal bone resorption and its effects on implant success. While a thorough understanding of the principles affecting implant placement is essential the ultimate goal of the dental practitioner must be patient satisfaction by providing an esthetic restoration which incorporates the best possible balance between long term function and esthetics.

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