OSSEOINTEGRATION OF DENTAL

IMPLANT IN OSTEPOROSIS
CONDITION
Achmad Aghasy1
Fajar Kurniawan1
1Master Student of Dental Science, Faculty of Dental Medicine, Airlangga University,
Surabaya – Indonesia
BACKGROUND

 Dental implants have become a more common treatment for replacing missing
teeth.1
 Consequently, in clinical dentistry, dental implants aim to increase patient satisfaction in
terms of improved chewing efficiency, physical health, and esthetics
 The favorable clinical performance of dental implants has been attributed to their firm
bone integration.
 Brånemark introduced the term “osseointegration” to describe the successful outcome of
bone-to-implant integration
 Clinically, the process of osseointegration reflects the mechanical anchorage of a dental
implant into the jaw bone that persists under all normal conditions of oral function
 Overall, bone regeneration related to dental implants in a healthy condition is a complex
process and can take up to several weeks.
 A few days after implantation, several biological events (bone regeneration) are
regulated by several growth and differentiation factors that are released in the implant
vicinity
 Although the survival rate of dental implants over a 10-year observation
has been reported to be higher than 90% in totally edentulous jaws6, dental implants
do fail in some patients
 There are many reasons for dental implant failure including an inappropriate diagnosis
and treatment inadequate information on the patient’s medical history, or lack of
experience and surgical skills to place dental implants correctly.7
 Most importantly, the clinical outcome of implant treatment is challenged in compromised
bone conditions, as are frequently present in elderly patients
 For example, epidemiological data show that osteoporosis is increasing among the elderly
female and male (>65 years) population
 A striking characteristic of the osteoporotic condition is the severe reduction of bone
quality and quantity which is suggested to be detrimental for bone–implant integration.9
 Additionally, the biomechanical characteristics of osteoporotic bone do not offer proper
stability to implants, being similar to type-IV bone (Figure 1), in which a decreased clinical
fixation of implants has been clearly demonstrated.
 Although research on osteoporosis is ongoing, including prevention and treatment
modalities, the knowledge on bone-biomaterial regeneration in osteoporotic bone
remains limited.
 However, the search for improved bone regeneration in challenged conditions has
helped propel the continuing evolution of modern dental implants
 Thus, decreased osteogenic capacity of bone in an osteoporotic condition can be
considered as a possible risk factor for implant failure.
 Such a risk of implant failure in osteoporotic bone is hypothetically related to various
factors that compromise bone–implant healing and potentially impair osseointegration
 Osteoporosis is a condition characterised by decreased bone strength
that culminates in an increased risk of fractures in response to minimal or low
velocity force.12
 Its prime fracture regions are around the vertebrae, hip and distal radius, though
fractures can occur at almost any skeletal site.13
 In general, most fragility fractures occur at non vertebral sites where bone is composed
mainly by compact or cortical tissue that accounts for 80% of the total bone mass of
an adult skeleton, whilst trabecular tissue makes up the remaining 20%.
 Osteoporosis is classified into primary and secondary osteoporosis on the basis of
the precipitating factors
This review will seek to appraise existing literature in this
field in an effort to better understand the interaction
between the immune system and the
skeletal system, with a particular focus on the role of
autoantibodies in osteoporosis development and how
dental implant can manage to fit and integrated to
human body that affected with osteoporosis.
THE IMMUNE SYSTEM AND BONE
HOMEOSTASIS

 the skeleton exists in a dynamic equilibrium characterized by continuous osteoclast-

mediated bone resorption and osteoblast-mediated bone deposition.21,23,24
 The latter biological process, termed “bone remodelling”, occurs in a harmonious and
simultaneous fashion, resulting in a negligible change in bone mass
 Briefly, bone remodeling follows the activation-resorption-formation (ARF) sequence.26
 The first step, called the activation phase, begins with stimulation of quiescent osteoblasts.
 the latter release key osteoclast differentiation factors triggering preosteoclast
fusion and differentiation to multinucleated osteoclasts marking the end of the activation
phase.23,26
 Once differentiated, osteoclasts polarize, adhere to the bone surface, and dissolve bone as
part of the resorption phase. They then undergo apoptosis, as a means to prevent
excessive bone resorption.23,25
 After this resorptive process, there is
an intermediate phase preceding bone formation, called a reversal
phase. At this time, some macrophage-like uncharacterized mononuclear
cells are observed at the site of remodeling, whose function consists of removal of
debris produced during matrix degradation.27
 The final phase termed bone formation is triggered by several growth factors stored in
the bone matrix and released after its degradation, which are likely to be responsible for
recruitment of osteoblasts in the resorbed area.24,27 Once recruited, osteoblasts produce
new bone matrix, initially not mineralized (osteoid), and then they promote its mineralization,
thus completing the bone remodeling process.24
 Both cortical and trabecular bone undergo a continuous process of structural remodeling as a
means of maintaining mineral homeostasis, adapting to mechanical changes and repairing
damage to bone.
 osteoclasts have been identified to derive from the same myeloid precursor cells
that give rise to macrophages and myeloid dendritic cells
 bone forming osteoblasts are noted to derive from mesenchymal stem cells.
 The coordinated stimulation of osteoclasts by osteoblasts and reciprocal activation of
osteoblasts by osteoclasts is referred to as coupling.24
 It is widely acknowledged that the complementary regulatory activities
of osteoclasts and osteoblasts are continuously controlled through
direct cell to cell contact, via extracellular matrix interaction
as well as by a variety of cells of the immune system
 Osteoclasts represent the sole bone-resorbing cells in
the body and are derived mainly following stimulation by two essential cytokines: the
macrophage colony- stimulating factor (M-CSF) and the receptor activator of nuclear factor-
kappa beta (RANK) ligand (RANKL), produced by osteoblasts.
 Though the RANK/RANKL pathway represents the central process through which bone loss is
regulated, there exist additional costimulatory pathways that are capable
of modifying the net outcome resulting from bone remodelling

 Additionally, a number of other cytokines are also reported to play a

role in osteoclastogenesis. For example, tumor growth factor beta
(TGFβ) is implicated in the enhanced recruitment of osteoblast pro-
genitor cells to sits of bone resorption, whilst, tumor necrosis factor-α
(TNF-α), is believed to facilitate the trafficking of osteoclast precursors
from bone marrow to lymphoid organs
THE IMMUNE SYSTEM AND BONE DISEASE

 Perturbation of homeostatic bone remodeling resulting in reduced bone strength

and subsequent fracture as a result of accelerated bone loss is closely linked to bone
diseases such as osteoporosis
 Firstly, low BMD and osteoporosis are commonly observed amongst individuals
living with the Human Immunodeficiency Virus (HIV)
 rapid bone loss and increased fracture risk are implicated in a range of autoimmune
diseases such as rheumatoid arthritis (RA), ankylosing spondylitis, psoriatic arthritis (PSA),
inflammatory bowel disease (IBD), and systemic lupus erythematous (SLE)
 In this regard, it is important to note that the profile of cytokines noted to be elevated in
conditions such as RA and ankylosing spondylitis characterized by osteoporosis, are
the same as those implicated in bone modulation, such as TNFα and IL-6.
AUTOIMMUNITY AND OSTEOPOROSIS

 Autoantibodies have been increasingly implicated

in the pathological bone loss characteristic of conditions such as osteoporosis
 Clinical studies comprising autoimmune disease samples have illustrated the ability of
autoantibodies to induce osteoclast differentiation and activation as
well as alter bone mineral content.
 autoantibodies such as rheumatoid factor (RF) and anti citrullinated protein (ACPA)
are identified as independent risk factors for the development of bone
erosions and osteoporosis in RA
DESIGN OF DENTAL IMPLANTS AND
PRIMARY STABILITY

 Dental implants mostly possess a threaded cylindrical or conical(root)-design (Figure 2).

The design parameters primarily affect load (i.e., stress/strain) distribution in the
bone tissue, resulting in a proper implant fixation and function
 These include implant diameter and length as well as thread pitch, shape, and depth.
Additionally, the presence of threads increases the surface area for osseointegration, and
thereby aids in the achievement and maintenance of direct bone-implant integration
THE IMPORTANCE IN SURGICAL-
IMPLANTATION TECHNIQUES

 Conventionally, the placement of dental implants sacrifices much bone tissue during the
drilling procedure, which is performed with a consecutive series of surgical drills to prepare an
implant bed fits the implant exactly
 Consequently, several modalities of implantation techniques have been proposed to optimize
a high degree of implant stability without removing additional bone, especially in situations
where limited bone density (i.e., challenged condition) is available
 Additionally, the 'undersized drilling' technique has been also explored extensively and most
implant manufacturers are currently recommending the undersized drilling technique for
implant placement.112
 In this procedure, bone density is locally optimized by lateral bone compression along the
implant sides using a final drill diameter considerably smaller than the implant diameter. This
method has resulted in higher insertion torque values, which, in tum, are the indicator of
improved primary implant (mechanical) stability.
PHYSICOCHEMICAL SURFACE
MODIFICATIONS FOR DENTAL IMPLANTS

 The osseointegration process relates to the all biological interactions between the host
bone and implant surface. In view of this, implant surface modification is considered as an
important approach to favor this process (Figure 3)
 Implant surface modification enhances the interactions with biological fluids and cells and
accelerates peri-implant bone healing as well as improves osseointegration at sites that
lack sufficient quantity or quality of bone
 implant surface micro-roughness offers an advantage as the area of contact is enlarged,
which plays a significant role in anchoring cells and connecting to surrounding tissues,
thereby favoring peri-implant osteogenesis.114
 Different methods have been developed to modify implant surface micro-roughness, of
which grit-blasting, acid etching, or combinations are most commonly used.
 Grit-blasting is performed by projection of silica (sand-blasting), hydroxyapatite, alumina,
or titanium oxide particles, and is followed commonly by acid-etching to homogenize the
micro-profile of the implant surface and to remove as much of the residual blasting
particles as possible.
 Acid-etching is often performed using hydrofluoric, nitric, sulfuric acid or combinations
thereof.115 Recently, the modification of the implant surface at the nanoscale level has
been also introduced, which is based on the assumption that mimicry of the nano-patten,
of bone structures might increase the surface energy-and hence improve matrix protein
adsorption, bone cell migration, and proliferation-and finally enhance osseointegration
DRUG-BASED IMPLANTS MODIFICATION

 new coating strategies to improve implant osseointegration involve the development of a

dedicated drug-loading ability to locally target bone disorders around dental implants more
effectively.125
 For instance, antiresorptive (e.g., bisphosphonates) and anabolic (e.g., strontium ranelate
and statins) agents might improve implant osseointegration in osteoporotic bone.126
 When these pharmacological drugs are incorporated onto the surface of implant, and released
gradually and locally in the peri-implant area, the bone healing process might be improved
 there are many methods to modify implant performance by improving the bone response
physically, chemically, or therapeutically.
 However, the exact underlying biological mechanisms of these methods
have not been fully characterized.
 Consequently, research has to focus on the in vivo investigation of existing implant surface
modifications in order to achieve the desired biological responses, especially in compromised
conditions.
EXPERIMENTAL MODELS FOR
DENTAL IMPLANTS

 For the investigation of the osseointegration of bone implants with a newly developed
surface modification, animal experiments are of fundamental significance.
 Several animal models are commonly used to study osseointegration (i.e., peri-implant
osteogenesis).128
 However, to explore the biological efficacy of an implant surface designed to be applied
in a compromised health condition, a specific animal model is needed resembling the
medical condition being investigated which is capable of demonstrating a relevant
biological response prior to clinical use.
CONCLUSION

 The mechanisms through which autoantibodies may mediate their effects remain
poorly understood.
 research suggests an independent function for these immune markers in the deterioration
of bone structure and resulting fragility fractures.
 The role played by autoantibodies in mediating immune processes driving osteoporosis
pathogenesis carries significant implications for better skeletal preservation by reducing
fracture rates and increasing BMD, particularly amongst older, postmenopausal
females known to be at a significantly greater risk of developing this disabling condition.
 Furthermore, research has revealed the occurrence of preferential alteration
of bone tissue when comparing the deterioration of micro- architecture between
trabecular and cortical bone.
 the influence of the immune system of differing bone tissue remains poorly understood.
 There is a clear need for prospective based population studies aimed at not only ascertaining
the impact of auto-
antibodies on accelerated bone loss characteristic of osteoporosis, but to understand the differing
effects of autoimmune processes on differing bone tissue between anatomic sites as well.
 The developments regarding implant surface modifications seem critical for bone healing and im
proving osseointegration at sites that lack sufficient quantity or quality of bone.