| Sažetak | Medikamentozna osteonekroza čeljusti označava odumiranje koštanog dijela čeljusti kod
pacijenata koji uzimaju antiresorptivnu terapiju, antiangiogene lijekove ili druge novije
lijekove čija se povezanost s nastankom osteonekroze čeljusti još istražuje. Lijekovi koji se
najčešće dovode u vezu s nastankom osteonekroze čeljusti su antiresorptivni lijekovi:
bisfosfonati i denosumabi. Mehanizam djelovanja ovih lijekova je inhibicija funkcije
osteoklasta, uz očuvanje funkcije osteoblasta i samim time povećanje koštane mase. Koriste
se u liječenju koštanih poremećaja, najčešće osteoporoze, kod multiplog mijeloma ili kod
pacijenata oboljelih od malignih bolesti. Medikamentozna osteonekroza isključivo pogađa
čeljusne kosti, najvjerojatnije zbog visoke stope remodelacije kosti, tanke sluznice i
prisutnosti velikog broja mikroorganizama u usnoj šupljini. Postoje različite teorije o nastanku
MRONJ-a, to su inhibicija resorpcije i remodelacije, upala i infekcija, inhibicija angiogeneze,
toksičnost mekih tkiva, imunološka disfunkcija i niske vrijednosti pH. Rizični čimbenici za
nastanak MRONJ-a su način primjene lijeka, doza, potentnost lijeka i trajanje terapije, a
uvjetovani su osnovnom bolesti pacijenta. Ostali su sistemski čimbenici: osnovna bolest,
kemoterapija, radioterapija, terapija kortikosteroidima, šećerna bolest, anemija i drugo. U
rizične lokalne faktore ubrajamo ekstrakciju zuba, parodontitis, ugradnju dentalnih implantata
i neadekvatno izrađene proteze. Bitan su također faktor navike pacijenata poput pušenja te
održavanje oralne higijene. S obzirom na kliničku sliku postoje četiri stadija MRONJ-a o
kojima ovisi liječenje bolesti. Glavni je cilj liječenja podići kvalitetu pacijentova života.
Nekrotični se dio kosti najčešće odstranjuje kirurškim putem, u terapiju se uključuju
antibiotici, a nastali defekt sanira se na različite načine. Danas se koriste i adjuvantne terapije
kao što su primjena lasera, autolognih faktora rasta i hiperbarične oksigenacije |
| Sažetak (engleski) | Medication-related osteonecrosis of the jaw (MRONJ) represents dying of the jawbone tissue
in patients receiving antiresorptive therapy, anti-angiogenic drugs or other newer medicines
whose link to the development of osteonecrosis of the jaw is still being investigated. Drugs
most commonly associated with osteonecrosis of the jaw are antiresorptive drugs:
bisphosphonates and denosumab. The mechanism of action of these drugs is to inhibit
osteoclast function, while preserving osteoblast function and, consequently to increase bone
mass. They are used in the treatment of bone disorders, most commonly osteoporosis,
multiple myeloma or with patients with malignant diseases. Medication-related osteonecrosis
exclusively affects the jawbone, most likely due to high rates of bone remodelling, thin
mucous membranes and the presence of a large number of microorganisms in the oral cavity.
There are different theories about MRONJ occurrence, and some of them are as follows:
resorption and remodelling inhibition, inflammation and infection, angiogenesis inhibition,
soft tissue toxicity, immune dysfunction, and low pH levels. Risk factors for the onset of
MRONJ are the mode of drug administration, dose, potency of the drug and the duration of
therapy, conditioned by the patient's underlying illness. Other systemic factors include:
primary disease, chemotherapy, radiotherapy, corticosteroid therapy, diabetes, anemia, etc.
Local risk factors include tooth extraction, periodontitis, dental implants placement, ill-fitting
dentures. The patient’s habits, such as smoking and maintaining oral health, are regarded as
an important factor. According to the clinical manifestations, there are four stages of MRONJ,
which the treatment of the disease depends on. The main goal of treatment is to raise the
quality of the patient's life. The necrotic part of the bone is usually surgically removed,
antibiotics are used in therapy, and the resulting defect is repaired in various ways. Adjuvant
therapies are also used today, including laser, autologous growth factors and hyperbaric
oxygenation. |
