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种植体周围软组织炎症
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来自 The University of Hong Kong 的课程
口腔种植学 （Implant Dentistry）
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从本节课中
种植牙的术后、未来的发展
种植体毫无疑问是“高维护”设备！在这个模块中，我们将讨论如何设计个性化，循证的策略，以保持种植体的长期健康和功能。我们还将回顾最常见的技术和生物学并发症，并讨论预防策略，早期诊断和管理技术。同时，我们将探讨一些尖端的技术和新趋势，包括在组织工程和再生中使用数字技术，在植入程序中使用动态导航和数字化工作流程等，这些趋势可能改变种植牙的未来。
与讲师见面
Nikos MattheosClinical Associate Professor in Implant Dentistry
The University of Hong Kong
There is a sequence of events
that leads to the chain reaction
of peri-implant inflammations.
The first step is contamination.
Bacteria of the mouth will populate
the exposed implant surfaces
almost within minutes after implant placement.
Infection, the second stage,
is defined as the active multiplication of bacteria
on a tissue or surface.
And the bacteria will start to multiply
on the exposed implant components
within the first few hours.
If bacteria are left to multiply uninterrupted,
they will create a biofilm,
which will soon increase in complexity and thickness.
If the biofilm matures, then the tissues
will respond with inflammation,
which we will diagnose clinically as peri-implant mucositis.
The role of the biofilm in the development
of peri-implant mucositis
is documented in numerous studies,
including a couple of studies
of experimental mucositis in humans.
In these studies, it took three weeks of complete absence
of oral hygiene for peri-implant mucositis
to develop in patients.
If the biofilm is removed at this stage,
the peri-implant tissues can return to health.
If the biofilm persists however,
transition to the peri-implantitis,
the final stage of inflammation, is very likely.
Peri-implantitis, the condition where implants
are losing supporting bone due to inflammation
is today a major therapeutical challenge.
As a new disease entity, the prevalence of peri-implantitis
is not easy to define and estimations vary
depending on the sensitivity of the diagnostic indicators used.
Although some authors have estimated peri-implantitis
to affect as many as 40% of the patients
after 10 years with implants,
the majority of studies place peri-implantitis
between 5-20% of patients for the same period.
It is also clear that the occurrence
of plaque-induced inflammation greatly depends on
the oral hygiene and the maintenance of the patients,
and consequently, the prevalence will be very low
in well-maintained patient populations.
The diagnosis of peri-implantitis is mainly clinical.
First, as we discussed previously,
start by continuously assessing the risk of your patients.
Patients with compromised oral hygiene,
smokers, patients with diabetes mellitus,
or history of periodontitis,
are also in higher risk to develop peri-implantitis.
Second, probe around the dental implants
at every maintenance appointment.
Bleeding on probing with light force
is an indication of inflammation.
Unlike teeth however, there is no
definitive pathological probing depth around implants.
As we often place implants rather deep in the tissues,
especially in the aesthetic zone,
probing depths of 4 or 5 mm
are not uncommon around healthy implants.
Therefore, compare the probing depths
at follow up with that at baseline,
when the implant was first restored.
Any increase in probing depth
might indicate initiated peri-implantitis.
Finally a periapical radiograph with parallel cone
can confirm the clinical diagnosis
if we can see evidence of marginal bone loss.
Bone loss around implants in peri-implantitis
follows typically a uniform circumferential pattern
that often resembles a crater.
The treatment of peri-implantitis is
depending on our ability to remove the aetiological factor
and maintain thereafter healthy conditions
for the peri-implant tissues.
Consequently, plaque control is the first essential step.
Two important parameters here:
First, ensure that the patient can practice
an optimal level of oral hygiene,
and second, ensure that the design
of the prosthesis allows for good cleaning.
In a study by Serino et al,
peri-implantitis was diagnosed almost 10 times
more frequently when the implant prosthesis
would not allow full access to oral hygiene.
Very often, your very first step to solve the puzzle
of peri-implantitis is to modify the prosthesis.
In a case like this, inability to clean
under the implant bridge has caused a rampant inflammation
of the peri-implant tissues.
In such a case we have to send the prosthesis
back to the lab to trim the emergence profile
of the pontics and open the interdental spaces,
so that the patient can use
interdental brushes and super floss.
This step alone will not halt peri-implantitis,
but it can significantly reduce the inflammation burden
and the swelling and allow to proceed further
with the next step.
The second step is to remove plaque and calculus
or deposits from the implant and the prosthesis surfaces.
This is commonly an adequate treatment
for peri-implant mucositis and it will be initially done
with a combination of closed debridement and antiseptics.
Common devices for debridement
can be rubber-coated ultrasonic tips
or specially-made hand curettes, while common antiseptics
include chlorhexidine mouthrinse and gel.
Finally, in the case of peri-implantitis,
surgical treatment will be required in most cases
in order to access and decontaminate
the exposed implant surfaces.
This is usually done with an access flap,
where the implant surface can be disinfected
with mechanical or chemical agents.
In certain cases where the local anatomy allows,
regenerative or resective surgery can be applied.
In the case of resective surgery,
after the removal of the granulation tissue
and disinfection of the implant surface,
the bone is flattened in order
to allow the exposed implant surface
to be accessible by oral hygiene.
In the case of regenerative approach,
when the defect morphology allows,
after cleaning the defects are filled
with a bone substitute,
and then covered with a membrane
as directed by the guided bone regeneration techniques
we discussed in Module 4.
Peri-implantitis is, today,
a significant therapeutical challenge
and the major threat to the long term success
of dental implants.
Even with the best of our treatments,
complete resolution of the inflammation
is often not possible.
The most effective point to break the vicious circle
of inflammation is exactly where it starts,
at the biofilm.
Keep the level of oral hygiene high,
and your patients under a strict maintenance program
and you will see little of the problem.
