Etiologies and Risk Indicators of Peri-implant Diseases
Similar to periodontal diseases, the prime causative factor for peri-implant diseases
is dental plaque.[4] Periodontal health is influenced by various factors such as oral hygiene, genetic
and epigenetic factors, systemic health, and nutrition.[5]
[6] Peri-implantitis and periodontitis lesions both harbor Gram-negative anaerobic bacteria
compared with healthy sites. However, peri-implantitis has higher microbial diversity
than periodontitis.[7] Moreover, peri-implantitis is penetrated predominantly by inflammatory cells, B-lymphocytes
and plasma cells, and frequently lacks a protective tissue layer over the bone, which
is typically present in periodontitis. Histologically, peri-implantitis lesions were
twice as large and had more blood vessels and the infiltrate in the connective tissue
compared with perodontitis.[8] Peri-implantitis demonstrated a 97% higher matrix metalloproteinases (MMP) level,
such as MMP-8, which was only 78% greater in chronic periodontitis compared with healthy
gingiva.[9] Furthermore, peri-implantitis tissue contains extracellular matrix antibodies.[10] The disease progression rate is faster in peri-implantitis, which generates a faster
and more severe loss of bone compared with periodontal disease. A nonlinear form of
progressive bone destruction occurs over time in peri-implantitis, which maybe because
of the differences in microorganisms at the implant sites, the host's defense mechanism,
and absence of a periodontal ligament.[11]
[12]
Risk indicators are referred to as factors associated with peri-implant diseases.
However, to identify true risk factors, prospective studies are needed because there
are currently few such studies. Thus, the term risk indicators were used in most studies.
The identified risk indicators of peri-implant diseases are plaque, smoking, history
of periodontitis, implant design and surface roughness of the transmucosal portion,
residual cement, emergence angle >30 degrees, radiation therapy, width of the keratinized
tissue and function time of the implant, sex, and diabetes.[13]
[14]
[15]
[16]
[17] In addition to these, other factors associated with peri-implantitis are occlusal
overload,[18] history of implant failure, patients’ parafunctional habits, and improper implant
position.[19]
[20]
[21] Peri-implant mucositis is associated with an increased risk of becoming peri-implantitis.
However, there are limited data available to support any systemic conditions as risk
indicators for peri-implant mucositis. Limited evidence has shown the correlation
of peri-implant diseases with alcohol consumption. Systemic diseases such as scleroderma,
ectodermal dysplasia, lichen planus, osteoporosis, rheumatoid arthritis, and Sjögren’s
syndrome may have negative effects on peri-implantitis and implant success.[15]
[22] To confirm these findings, additional detailed studies are needed. Genetic traits
may be correlated with peri-implant diseases; however, the results are conflicting
and limited.
Prosthetic restorations are associated with peri-implant diseases. There are three
types of implant–abutment connections: platform-switched, butt-joint, and no interface.[19] Bone loss of approximately 1.5 to 2.0 mm may occur with butt–joint connections due
to the micro gap, which is wide enough for bacterial penetration and colonization.
Although platform switching prevents or reduces marginal bone loss,[20] contaminated connections can cause peri-implantitis and implant failure over time.
Moreover, a convex restoration profile creates an additional risk for bone-level implants.[15]
Retained cement left on the implant surface after crown cementation is a potential
risk for peri-implantitis because retained cement has an adverse effect on peri-implant
tissues ([Fig. 3]).[14]
[23] The position of the implant, such as too apical or angled, and an overcontoured
crown, negatively affect the accessibility for removing excess cement from the subgingival
space. An implant splinted to both a mesial and distal adjacent implant has a higher
risk of peri-implantitis.[24] Cement causes roughness, favors bacterial attachment and foreign body reactions,
and results in peri-implantitis. Removing the cement results in the resolution of
inflammation in a few days to weeks and can be done using a closed procedure (dental
endoscope) or open surgical flap procedure. Hence, to reduce the risk of peri-implant
disease associated with excess cement, it is recommended that the crown margin is
at the level of the mucosal margin, providing sufficient access and soft-tissue maturation,
and early follow-up evaluation after restoration placement should be done.[14]
Fig. 3 Retained cement results in peri-implantitis: (A) retained cement at the crown margin and excess cement in the peri-implant inflamed
tissue, and (B) excess cement around the abutment. Reproduced from Ref.[23] with permission from John Wiley & Sons A/S.
Mechanical stress beyond the threshold (occlusal overloading) is also considered a
major cause of screw loosening or implant body fracture or other components. Increased
mechanical stress can result in a greater concentration of force on the cervical part
of the implant.[25]
[26] Furthermore, overloading and increased loading time cause fatigue microdamage that
results in bone resorption which may, in turn, progress to peri-implantitis.[27] Moreover, increased bone remodeling around the implant is seen when the implant
is subjected to high-loading forces. Mutually protected occlusal schemes and favorable
contacts, avoiding cantilevers, narrowing the occlusal table, increasing implant number
when replacing teeth, decreasing cusp inclines, increasing contact points, and eliminating
parafunctional habits can reduce peri-implantitis.[28]
Peri-implantitis Treatment
Peri-implant diseases share similar clinical features and etiologies to periodontal
diseases; thus, similar treatment approaches have been adopted to manage them. However,
treatment outcomes vary. Mucositis treatment is more predictable; in contrast, peri-implantitis
treatment is difficult, and the outcome varies. Therefore, supportive therapy at the
initial stage reduces the risk of the onset of peri-implantitis.[30]
[31] Various treatments for peri-implant diseases are presented in [Fig. 4]. Peri-implant maintenance therapy or supportive therapy (SPT) increases the implant
survival rate.[32]
Fig. 4 Various treatments for peri-implant diseases.
An appropriate management strategy should consider local and systemic factors.[33] Long-term supportive therapy is recommended for peri-implant diseases. Its main
goals are infection control, prevent disease progression, and restore the lost bone.
This protocol underscores the routine follow-up of the implant patient with periodic
assessment of plaque and calculus, BOP, PD, and radiological evaluation for bone loss.
These parameters indicate disease severity and extent. According to the CIST protocol,
depending on the clinical and radiographic findings, different treatment approaches
are indicated.
Nonsurgical Treatment
The different nonsurgical therapy of peri-implant disease comprises mechanical, chemical,
antibiotics, lasers, and oral hygiene instruction.
Mechanical Methods
Mechanical debridement reduces inflammation by removing microbial plaque on the implant
surface. Mechanical instruments for plaque removal include plastic curettes, ultrasonic
scalers with a metal tip, metal curettes, air abrasive, and metallic (titanium) brushes
([Fig. 5]).[34] Piezoelectric scalers and hand instruments are also effective in reducing BOP score,
plaque index, and PD. Ultrasonic scalers with metal tips and metal curettes can eliminate
surface material down to 0.83 μm in size and efficiently remove bacteria.[35] However, these must be used carefully because they may create scratches on the implant
surfaces if used improperly.[36] Although plastic curettes are also available, they may not incompletely remove the
debris or biofilm. Mechanical plaque removal methods can be combined with antibiotics
or surgical methods for a better outcome. In a randomized trial, Toma et al[34] compared three mechanical treatments (air-abrasive device, titanium brush, and plastic
curettes,) for peri-implantitis. They found that the air-polishing device and titanium
brush were more efficient than the others; however, the success was low.
Fig. 5 Mechanical treatments of peri-implantitis: (A) plastic curettes, (B) air abrasive, and (C) metallic brush. Reproduced from Ref.[34] under the Creative Commons Attribution License (CC BY 4.0) from Frontiers Media
S.A.
Persson et al[37] performed a single-blinded, longitudinal, randomized study to assess the effects
of mechanical debridement on the peri-implant microbiota in peri-implantitis lesions
wherein they tested 79 different microorganisms. They found no microbiological differences
for implants treated with the ultrasonic device. Inconsistent changes occurred following
the first week. No microbiological differences were found for any species or between
treatment study methods in peri-implantitis between the baseline and 6-month samples.
They concluded that both methods failed to eliminate or reduce bacterial counts in
peri-implantitis. Moreover, the adjunctive use of antimicrobial mouth rinses enhances
the outcome of mechanical therapy in peri-implantitis.[38] Furthermore, surgical procedures (open flap debridement) increase the effectiveness
of mechanical treatment of peri-implantitis.[39] Hence, mechanical debridement alone may fail to eliminate bacteria and this treatment
should be combined with other treatments (antiseptics and surgical treatment).
Antiseptics
Antiseptics are mainly indicated for reducing bacterial counts and can be used in
the form of local irrigation. Chlorhexidine (CHX) gluconate is commonly used in periodontitis
and peri-implant diseases. CHX retards bacterial colonization and its 0.12% concentration
effectively reduces peri-implantitis disease.[40]
[41] Hence, CHX is useful as an antiseptic agent in peri-implantitis. Furthermore, local
and controlled release using CHX chips aids in periodontal re-osseointegration; however,
there are few clinical studies. Hence, further clinical studies on its application
for bone re-osseointegration in peri-implantitis are needed.
CHX has specific disadvantages because clinically used 2% CHX permanently halts cell
migration and significantly reduces fibroblast, myoblast, and osteoblast survival
in vitro.[42] Thus, further in vivo studies are required to examine and optimize CHX safety and efficacy.
Antibiotics and Antimicrobial Agents
Antibiotics are used in adjunct to mechanical therapy because they act against infection,
either by inhibiting or killing the infectious agent. Different local and systemic
antibiotic applications have been investigated. In peri-implantitis, the most commonly
used local antibiotics are minocycline (MNO), doxycycline, gentamicin, and cefazolin.[43]
[44]
[45]
Local application of doxycycline or MNO following debridement and irrigating with
an antiseptic agent is useful in treating moderately deep lesions.[43] Cha et al[44] evaluated the clinical, microbial, and radiographic effects of local MNO combined
with surgical treatment of peri-implantitis. They found that repeated local delivery
of MNO combined with surgical treatment provides increased clinical parameters and
radiographic bone fill, with a higher treatment success rate in the short-term healing
period. Furthermore, various polymeric films with antibiotics such as tetracycline
hydrochloride polylactic acid, poly(e-caprolactone), and polymer/tetracycline-containing
solutions, reduce peri-implantitis development and associated pathogens.[46] Local antibiotics, such as MNO, doxycycline, or CHX, are effectively combined with
mechanical treatments for peri-implantitis, especially for incipient to moderate lesions.
MNO and doxycycline have shown better results compared with CHX. Moreover, the combination
of systemic antibiotics (such as ceftriaxone or gentamycin) and local antibiotics
(tobramycin or gentamycin) demonstrate better treatment results.
Systemic antibiotic therapy increases the host defense to eliminate the infection
by combating subgingival pathogens that remain following mechanical therapy. The combination
of antibiotics (local and systemic) can be more beneficial in peri-implant infections.
Furthermore, systemic antibiotic prophylaxis by injecting antibiotics at the lesion
lowers the risk of postoperative infection. The surgical treatment of peri-implantitis
can be combined with hydrogen peroxide and systemic antibiotics. A study found that
the surgical treatment of peri-implantitis is effective and that therapy outcomes
are affected by implant surface characteristics.[47] However, the benefits of systemic antibiotics are not sustained for over 3 years.
Carcuac et al[48] investigated the adjunctive use of systemic antibiotics and the local use of CHX
for implant surface decontamination in peri-implantitis. They found that the treatment
was successful in 45% of all implants but was higher in implants with an unmodified
surface (79%) compared with those with a modified surface (34%). The local use of
CHX had no overall effect on treatment outcomes. Although adjunctive systemic antibiotics
had no impact on treatment success at implants with an unmodified surface, a positive
effect on treatment success was observed at implants with a modified surface. There
is a likelihood for treatment success, using adjunctive systemic antibiotics, in patients
with implants with a modified surface; however, it was low. Hence, after careful assessment,
it is recommended to use antibiotics to treat peri-implantitis.
Antimicrobial photodynamic therapy (aPDT) has emerged as a promising alternative to
promote bacterial elimination and crestal bone remodeling in peri-implantitis.[49] This technique is performed using direct mechanical debridement, followed by aPDT
using 200 μg/mL methylene blue under red laser irradiation, which decontaminates the
implant surface and surrounding tissue. Similarly, bioactive glass (BAG), especially
Bioglass 45S5 and S53P4, are efficient antimicrobial agents, and their properties
make BAG perhaps the ideal bone substitute for treating peri-implant infections.[50]
Surface Decontamination
Nonsurgical mechanical therapy has a predictable outcome in peri-implant mucositis
cases. However, it is more challenging when implant surfaces are exposed in peri-implantitis
cases. Mechanical debridement alone may not completely remove the plaque because the
instruments cannot access between the implant threads.[51] Adjunctive treatments are proposed for surface decontamination to increase the efficiency
of the nonsurgical treatment of peri-implant diseases.
Chemical Methods
Chemical methods include the local delivery of antibacterial agents. Commonly used
chemicals for treating peri-implant diseases are described below.
Citric Acid (CA)
Although CA is used for cleaning implants, it is also the chemotherapeutic agent with
the highest potential for removing the biofilm from contaminated Ti surfaces in vitro; however, it does not achieve complete removal.[52] Currently, the bactericidal effect of CA against biofilms has not been investigated
on Ti surfaces. Burnishing with CA (pH = 1) for 1 minute significantly decreased the
amount of E. coli lipopolysaccharide (LPS) on grit-blasted Ti alloy surfaces.[35] Gosau et al[53] performed a clinical study to evaluate the efficacy of six antimicrobial agents,
sodium hypochlorite (NaOCl), Hydrogen peroxide (HP) 3%, CHX 0.2%, Plax (triclosan),
Listerine, and 40% citric acid on the surface decontamination of an oral biofilm attached
to titanium implants. They found that the total bacterial load on the Ti surfaces
was significantly higher in the control solution, phosphate-buffered saline, after
incubation compared with the antiseptic groups. Hence, all tested antiseptics reduced
microorganisms accumulated on the Ti surfaces. Moreover, CA and Plax had a significantly
lower bactericidal effect against bacteria compared with NaOCl, HP, CHX, and Listerine.
CA toxicity has been investigated. CA at 4 to 10% concentrations did not demonstrate
toxic effects on human osteoblasts.[54] In contrast, 40% CA (pH 1) for 30 to 60 seconds may have a toxic effect on the peri-implant
tissues and the implant and abutment junction due to its acidic pH. Hence, we need
more clinical studies on how to effectively apply CA in order to avoid tissue contact.
Ethyldiaminetetraacetic Acid (EDTA)
The use of EDTA in dentistry is primarily as a chelating agent to eliminate the smear
layer for periodontal regeneration and peri-implantitis. Wohlfahrt et al[55] debrided 32 peri-implantitis defects with Ti curettes, cleaned them with 24% EDTA
for 2 minutes, and rinsed them with saline and found that the EDTA reduced the PD
by 2.6 mm. Furthermore, Kotsakis et al[56] treated implant surfaces with 20% CA, 0.12% CHX, 24% EDTA, 1.5% sodium hydrochloride,
or sterile saline (control). Their results demonstrated that the bacterial counts
were significantly reduced after the decontamination and use of the chemotherapeutic
agents. However, the agent residue caused some cytotoxic effects compared with control.
Thus, EDTA should be used for treating peri-implantitis with caution.
Hydrogen Peroxide (HP)
Hydrogen peroxide is effective in decreasing the number of bacteria and fungi, for
example, C. albicans, S. sanguinis or S. epidermidis from Ti specimens.[57] Rubbing implants with 3% HP for 1 minute significantly decreased the E. Coli LPS from grit-blasted Ti alloy and HA-coated strips versus the untreated samples.[35] Similarly, another study found that 10% HP inactivated the human biofilm and removed
99.9% of the bacteria from the implant surface.[52] Moreover, 10% HP (swabbing for 1 minute) can also be used to clean the implant surface,
which resulted in re-osseointegration in peri-implantitis lesions. However, HP is
extremely reactive and may harm oral tissues if they are exposed to high-strength
HP for a prolonged duration. Thus, HP should be used in treating peri-implantitis
with caution.
Saline
Cleaning the implant surface with curettes and saline generates clinically stable
results in peri-implantitis. Surgically debriding the implant with curettes, followed
by rinsing with sterile saline and postoperative antibiotics (amoxicillin and metronidazole)
prevents the advancement of peri-implantitis. A study found that postoperative amoxicillin
resulted in an increased number of resistant anaerobes and a decreased number of sensitive
facultative bacteria and facultative Gram-positive cocci compared with placebo; however,
there were no signs/symptoms of infection in any group.[58]
The use of adjunct chemical agents may improve the ability of saline to decontaminate
the implant surface. However, a significant clinical benefit has not been demonstrated.
Currently, there are still no conclusive studies showing the benefit of any of these
agents compared with the other.
Simulated Radiation Emission (Lasers)
Stimulated radiation emission has demonstrated a beneficial therapeutic effect in
peri-implantitis and can be used to support conventional mechanical therapy.[59] The advantages of laser treatment include patient comfort, pain relief, and better
results for specific applications.[60] The various lasers investigated for treating peri-implantitis are erbium-doped yttrium
aluminum garnet (Er:YAG) laser, diode laser, and carbon dioxide (CO2) laser.[61] Laser therapy, in combination with nonsurgical or surgical therapy for treating
peri-implant diseases, provided minimal benefit in PD reduction, clinical attachment
level gain, recession reduction, and plaque index reduction.[62] Lasers, when used as an adjunct to nonsurgical therapy, might result in more BOP
reduction over the short-term.
Laser application in peri-implant areas results in the activation of cellular photoreceptors
(cytochrome C oxidase) absorbing the laser radiation and delivers it to the cell’s
mitochondria. This increases the cell’s adenosine triphosphate, which is the product
of cytochrome C oxidase and the Krebs cycle, level, and increases cellular activity.[63] Increased adenosine triphosphate stimulates macrophages, fibroblasts, mast cells,
endothelial cells, bradykinin, nerve cells, and growth factors, which increase collagen
synthesis, resulting in tissue regeneration.
The Er:YAG laser settings used in treating peri-implantitis are 100 mJ/pulse, 1 W,
10 Hz, and 12.74 J/cm2 for 60 seconds.[64] Care should be used when using an Er:YAG laser 2940 nm wavelength to avoid adverse
thermal effects on the implant surface. In a clinical study, Clem and Gunsolley[65] evaluated the effective treatment regime for peri-implantitis lesions with deep
(≥ 6 mm) defects using an Er:YAG laser for implant surface decontamination, removing
defect granulomatous tissues, and grafting therapy for bony defect resolution. They
found that the mean PD was reduced by approximately 3.5 mm at 12 months and remained
stable (mean 3.2 mm 12 months later). Radiographically, PDs were reduced due to peri-implant
defect bone fill. Similarly, Yoshino et al[66] found that antibiotic therapy significantly reduced the bacterial amount from the
peri-implantitis sites and that Er:YAG laser therapy, along with bone augmentation,
enhanced bone regeneration in the peri-implant bone defects.
The use of a low-intensity diode laser increased soft-tissue regeneration. Pai et
al[67] found that the clinical benefits of the laser supported other peri-implantitis treatments
in their case series. They demonstrated that a diode laser had positive effects when
treating peri-implantitis and dental implant osseointegration. Furthermore, a systematic
review showed that laser use resulted in similar PD reduction compared with conventional
mechanical debridement in the short-term.[68] In contrast, Kotsakis et al[69] recommended that laser therapy in peri-implantitis should be used as a phase I therapy.
Moreover, a combination of nonsurgical treatment using granulation tissue curettage,
laser detoxification, CHX irrigation, and MNO ointment injection resulted in bone
formation.[70] Hence, a combination treatment is essential for an effective outcome.
Similarly, CO2 lasers can be used to treat peri-implantitis.[61] Continuous wet CO2 lasers are more effective compared with dry CO2 laser in treating peri-implantitis. Because the clinical outcomes from CO2 lasers are unstable, these lasers are less commonly used and investigated. To determine
its clinical effectiveness, further clinical trials should be performed.
These results indicate that peri-implantitis can be treated effectively using lasers
with no damage to the surrounding tissues, but they also suggest that further investigations
are required to determine the clinical efficacy of laser treatment. In addition, future
research should focus on different types of lasers in clinical studies and long-term
clinical outcome.
Surgical Treatment
Surgical treatment allows access to clean the inflammatory lesion in peri-implantitis.
Surgical intervention therapy is recommended for treating peri-implantitis for a more
favorable outcome. Surgical treatment includes access flap and debridement, access
flap and bone recontouring or resective surgery, and regenerative approaches using
bone grafts with or without a membrane.[51] Implant surface decontamination is critical and often performed. Incomplete surface
debridement can obstruct bone regeneration on the previously exposed surface of diseased
implants. Surface decontamination can be achieved by various modalities, as previously
mentioned.
Jepsen et al[71] compared the effects of surgical treatment of peri-implant defects between using
open flap debridement (OFD) and OFD plus porous titanium granules (PTGs). The OFD
plus PTG group demonstrated a mean reduction in PD of 2.8 mm compared with 2.6 mm
in the OFD group. BOP reduced from 89.4 to 33.3% and from 85.8 to 40.4% for the test
and control groups, respectively. Besides, there was no significant difference in
the complete resolution of peri-implantitis because this was achieved in 30% of the
implants in the test group and 23% of the implants in the control group. Reconstructive
surgery using PTGs resulted in significantly enhanced radiographic defect bone fill
compared with OFD.
If nonsurgical treatment for peri-implantitis fails or if the peri-implant disease
is at the moderate or severe stage, surgical therapy can be considered. Surgical correction
of the PD and bone recontouring with plaque control is important in active peri-implant
disease.
Air-abrasive Powder (AP)
AP uses an abrasive powder of sodium bicarbonate, calcium phosphate, or the amino
acid glycine, which is driven by compressed air to eliminate the biofilm.[72]
[73] AP treatment efficiently cleans contaminated implant surfaces.[73]
[74]
Tastepe et al[75] evaluated AP treatment as an implant surface cleaning method for peri-implantitis.
They found that considerable re-osseointegration (39–46%) was achieved with improved
clinical parameters after treatment when used in combination with surgical treatment.
The treatment results are influenced by the powder type used, the application time,
and whether the powder was applied surgically or nonsurgically. They concluded that
the in vivo data on AP treatment as an implant surface cleaning method is insufficient to draw
definitive conclusions. These results were similar to the results obtained by Schwartz
et al,[74] who found that glycine AP was effective in treating mucositis, enhanced the efficiency
of nonsurgical treatment, and resulted in partial bone regeneration. Hence, clinicians
can consider using AP for implant surface cleaning in peri-implantitis treatment.
Debridement with air abrasion facilitates the mechanical removal of bacterial biofilms
but may damage implant surfaces on a microscopic level. Matsubara et al[72] investigated the cleaning potential of various APs and their effect on titanium
implant surfaces. They used three types of APs: sodium bicarbonate, glycine, and erythritol
for 60 seconds. They found significant differences in cleaning potential between the
groups. Sodium bicarbonate was the only powder that significantly increased implant
roughness on the implant collar (1.53—2.10 μm) and threads (3.53—4.20 μm). Although
the large-sized powder resulted in the greatest cleaning effect, it also caused more
alterations on the implant surface. Glycine and erythritol treatment displayed no
significant changes in surface roughness; however, they demonstrated a limited ink
removal capacity.
Resective Surgery
The objective of resective surgery is to reduce pocket depth utilizing osteoplasty
and/or ostectomy, correct the osseous defect, and allow better flap adaptation. In
addition to bone recontouring, implantoplasty (smoothening) of the implant surface
can be performed. An apically positioned flap combined with osteoplasty and implantoplasty
was effective and reliable in treating peri-implantitis; however, an increased gingival
recession may limit its use in esthetic areas.[76]
Implantoplasty
Implantoplasty, also known as fixture modification, is the process of removing an
infected, exposed implant surface. The goals of implantoplasty are to decontaminate
the infected implant surface and gain a smooth surface, which decreases plaque adherence.[77] Implantoplasty is usually performed together with resective osseous surgery and
an apically positioned flap. This procedure can be performed using a high-speed diamond
burr to remove the implant threads, followed by an Arkansas burr to polish the surface.
These burrs were found to be the most effective in generating the smoothest implant
surface.[78] Implantoplasty combined with ostectomy and osteoplasty is effective in eliminating
the progression of peri-implantitis. These results indicate that pocket removal with
bone recontouring and plaque control is effective in treating peri-implantitis.
The disadvantage of implantoplasty is the metal debris, which is generally cytotoxic
and genotoxic, from implants that often remain in the peri-implant tissues, which
may cause adverse effects. The physicochemical properties and concentration of the
debris determine the degree of the harmful effects. These effects can be prevented
using a rubber dam or bone wax to protect the soft tissue during the procedure. Implantoplasty
can also weaken the implant–abutment complex, especially in an implant less than 3.75
mm in diameter. A study found that implantoplasty significantly reduced the bending
strength of narrow implants, with no effect in wide implants.[79] Hence, implantoplasty should be done with caution on narrow implants and single
implants subjected to more occlusal load.
Regenerative Surgery
The regenerative approach attempts to regenerate bone around peri-implantitis sites.
The materials used are bone grafts, with or without membranes, or membrane alone.
Biologic agents, such as growth factors or bone morphogenic proteins, can be considered.[2]
Various types of graft materials with or without a collagen membrane are often used
for bone regeneration and bone augmentation. The bone graft acts as a scaffold; thus,
it may improve bone regeneration because the barrier membrane maintains the space
for cell infiltration and should be considered, especially in large defects. However,
previous studies did not demonstrate clinical benefits of using a membrane. A systematic
review demonstrated that regenerative treatment led to a 1.97 mm radiographic bone
gain, 2.78 mm PD reduction, and 55% decrease in the BOP. Using membranes and submerged
healing did not improve the clinical parameters.[80] Wiltfang et al[81] evaluated regenerative treatment using autologous and xenogeneic bone graft with
growth factors and found a reduced PD of 4 mm at the 1-year follow-up.
Various dental soft and hard tissues have been successfully regenerated in vitro using stem cells, indicating promising advancement in tissue engineering in dentistry.[82]
[83]
[84] Growth factors and stem cell therapies are also being used for tissue regeneration
in peri-implantitis cases. A study found that the recombinant human platelet-derived
growth factor resulted in a higher percentage (40%) bone fill, due to its osteoconductive
property, which subsequently increased the clinical attachment level compared with
β-tricalcium phosphate (β-TCP).[85] Acemannan sponges (Aloe vera extract) have generated bone formation in bone defects and may be used in peri-implantitis;
however, further clinical studies are needed.[86]
A bone graft with a membrane may facilitate space maintenance favoring bone regeneration.[87] Thus, this approach may provide the most favorable outcome. However, evidence has
shown that the regenerative approach for treating a peri-implant defect remains unpredictable.
Partial regeneration is possible in implant defects using various graft materials
with resorbable membranes after guided bone regeneration. However, nonresorbable membranes
have a disadvantage in that they must be removed by performing another surgery.
Surgical treatment may not be a good option in some peri-implantitis cases. When there
is a substantial loss of bone in peri-implantitis (half the length of the implant),
the success of surgery is unlikely.[88] Implants that are placed in an improper position can limit treatment outcomes. Additionally,
implant mobility indicates advanced bone loss (> 60%) or a lack of osseointegration
of the implant. In these cases, implant removal is recommended.[89] If implant removal is necessary, then the second implantation should be performed
with a larger diameter implant.[90]
