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Osteomyelitis often requires prolonged antibiotic therapy for weeks or months. A PICC line or central venous catheter can be placed for long-term intravenous medication administration. It may require surgical debridement in severe cases, or even amputation.
Initial first-line antibiotic choice is determined by the patient's history and regional differences in common infective organisms. A treatment lasting 42 days is practiced in a number of facilities. Local and sustained availability of drugs have proven to be more effective in achieving prophylactic and therapeutic outcomes. Open surgery is needed for chronic osteomyelitis, whereby the involucrum is opened and the sequestrum is removed or sometimes saucerization can be done. Hyperbaric oxygen therapy has been shown to be a useful to the treatment of osteomyelitis.
Prior to the widespread availability and use of antibiotics, blow fly larvae were sometimes deliberately introduced to the wounds to feed on the infected material, effectively scouring them clean. In 1875, American artist Thomas Eakins depicted a surgical procedure for osteomyelitis at Jefferson Medical College, in a famous oil painting titled "The Gross Clinic".
There is tentative evidence that bioactive glass may also be useful in long bone infections. Support from randomized controlled trials, however, is not available as of 2015.
Five bisphosphonates are currently available. In general, the most commonly prescribed are risedronic acid, alendronic acid, and pamidronic acid. Etidronic acid and other bisphosphonates may be appropriate therapies for selected patients but are less commonly used. None of these drugs should be used by people with severe kidney disease.
- Etidronate disodium The approved regimen is once daily for six months; a higher dose is more commonly used. No food, beverage, or medications should be consumed for two hours before and after taking. The course should not exceed six months, but repeat courses can be given after rest periods, preferably of three to six months duration.
- Pamidronate disodium in intravenous form: the approved regimen uses an infusion over four hours on each of three consecutive days, but a more commonly used regimen is over two to four hours for two or more consecutive or nonconsecutive days.
- Alendronate sodium is given as tablets once daily for six months; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).
- Tiludronate disodium are taken once daily for three months; they may be taken any time of day, as long as there is a period of two hours before and after resuming food, beverages, and medications.
- Risedronate sodium tablet taken once daily for 2 months is the prescribed regimen; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).
- Zoledronic acid is given as an intravenous infusion; a single dose is effective for two years. This is recommended for most people at high risk with active disease.
Calcitonin, also called calcitonin-salmon, is a synthetic copy of a polypeptide hormone secreted by the ultimobranchial gland of salmon. Miacalcin is administered by injection, three times per week or daily, for 6–18 months. Repeat courses can be given after brief rest periods. Miacalcin may be appropriate for certain patients, but is seldom used. Calcitonin is also linked to increased chance of cancer. Due to the increased risk of cancer, the European Medicines Agency (EMA) recommended that calcitonin be used only on a short-term basis for 3 conditions for which it had previously been approved in the European Union: Paget's disease, acute bone loss resulting from sudden immobilization, and hypercalcemia caused by cancer.
The EMA said it based its recommendations on a review of the benefits and risks of calcitonin-containing medicines. Conducted by the agency's Committee for Medicinal Products for Human Use (CHMP), the review encompassed available data from the companies that market these drugs, postmarketing safety data, randomized controlled studies, 2 studies of unlicensed oral calcitonin drugs, and experimental cancer studies, among other sources.
CHMP found that "a higher proportion of patients treated with calcitonin for long periods of time develop cancer of various types, compared with patients taking placebo." The increase in cancer rates ranged from 0.7% for oral formulations to 2.4% for the nasal formulation. CHMP concluded that the benefits of calcitonin for osteoporosis did not exceed the risks. The nasal spray's only indication is for osteoporosis, thus justifying the drug's removal from the market.
As a solution for injection or infusion, calcitonin should be administered for no more than 4 weeks to prevent acute bone loss resulting from sudden immobilization, and normally for no more than 3 months to treat Paget's disease, the EMA said. The agency did not specify a time frame for the short-term use of calcitonin for treating hypercalcemia caused by cancer.
The treatment should be tailored to the cause involved and the severity of the disease process. With oral osteoporosis the emphasis should be on good nutrient absorption and metabolic wastes elimination through a healthy gastro-intestinal function, effective hepatic metabolism of toxicants such as exogenous estrogens, endogenous acetaldehyde and heavy metals, a balanced diet, healthy lifestyle, assessment of factors related to potential coagulopathies, and treatment of periodontal diseases and other oral and dental infections.
In cases of advanced oral ischaemic osteoporosis and/or ONJ that are not bisphosphonates related, clinical evidence has shown that surgically removing the damaged marrow, usually by curettage and decortication, will eliminate the problem (and the pain) in 74% of patients with jaw involvement. Repeat surgeries, usually smaller procedures than the first, may be required. Almost a third of jawbone patients will need surgery in one or more other parts of the jaws because the disease so frequently present multiple lesions, i.e., multiple sites in the same or similar bones, with normal marrow in between. In the hip, at least half of all patients will get the disease in the opposite hip over time; this pattern occurs in the jaws as well. Recently, it has been found that some osteonecrosis patients respond to anticoagulation therapies alone. The earlier the diagnosis the better the prognosis. Research is ongoing on other non-surgical therapeutic modalities that could alone or in combination with surgery further improve the prognosis and reduce the morbidity of ONJ. A greater emphasis on minimizing or correcting known causes is necessary while further research is conducted on chronic ischaemic bone diseases such as oral osteoporosis and ONJ.
In patients with bisphosphonates-associated ONJ, the response to surgical treatment is usually poor. Conservative debridement of necrotic bone, pain control, infection management, use of antimicrobial oral rinses, and withdrawal of bisphosphonates are preferable to aggressive surgical measures for treating this form of ONJ. Although an effective treatment for bisphosphonate-associated bone lesions has not yet been established, and this is unlikely to occur until this form of ONJ is better understood, there have been clinical reports of some improvement after 6 months or more of complete cessation of bisphosphonate therapy.
Culture and sensitivity of the wound site determines the choice of antibiotic. Repeated culture and sensitivity testing is often carried out in OM since the treatment is prolonged and antibiotic resistance may occur, when a change in the drug may be required.
What happens after your child is diagnosed with CRMO/CNO?
Find a doctor who has experience with patients with CRMO/CNO. CRMO/CNO in children is generally treated by a pediatric rheumatologist. Ask your doctor for a referral.
Why do we treat CRMO/CNO?
- Reduce inflammation
- Prevent bone damage and bone deformities
- Decrease pain
How is CRMO/CNO treated?
CRMO/CNO is different for each patient. Not every child responds to every treatment. Your doctor may need to try several medications before finding the one that works for your child. In severe cases, doctors may combine medications to treat the disease. Your doctor will work with you and your child to help find the best treatment.
For some CRMO/CNO patients, the disease can be managed with non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs are the first line treatment. However, if NSAIDs are not effective, or if your child does not tolerate NSAIDs well, second line treatments are available.
First line treatments include Naproxen (Aleve), Celecoxib (Celebrex) Meloxicam (Mobic), Piroxicam (Feldene), Indomethacin (Indocin), Diclofenac (Voltaren).
Second line treatments include corticosteroids (Prednisone/Prednisolone), Methotrexate (Otrexup, Rasuvo, Trexall), Sulfasalazine (Azulfidine), Pamidronate (Aredia), Zolendronic Acid (Zometa), Adalimumab (Humira), Etanercept (Enbrel), Infliximab (Remicade).
These medications are also used in children with other inflammatory and/or bone conditions. Side effects may occur while taking these medications. Your physician will have a discussion with you prior to starting any new treatment.
Normally, asymptomatic cases are not treated. Non-steroidal anti inflammatory drugs and surgery are two typical options for the rest.
Mainly surgical approach has to be taken.
If cavity is small then surgical evacuation & curettage is performed under antibiotic cover.
If cavity is large then after evacuation, packing with cancellous bone chips
An infectious bone disease is a bone disease primarily associated with an infection.
An example is osteomyelitis.
Specific treatment for enchondroma is determined by a physician based on the age, overall health, and medical history of the patient. Other considerations include:
- extent of the disease
- tolerance for specific medications, procedures, or therapies
- expectations for the course of the disease
- opinion or preference of the patient
Treatment may include:
- surgery (in some cases, when bone weakening is present or fractures occur)
- bone grafting - a surgical procedure in which healthy bone is transplanted from another part of the patient's body into the affected area.
If there is no sign of bone weakening or growth of the tumor, observation only may be suggested. However, follow-up with repeat x-rays may be necessary. Some types of enchondromas can develop into malignant, or cancerous, bone tumors later. Careful follow-up with a physician may be recommended.
Treatment consists of rest, non-weightbearing and painkillers when needed. A small study showed that the nonsteroidal anti-inflammatory drug ibuprofen could shorten the disease course (from 4.5 to 2 days) and provide pain control with minimal side effects (mainly gastrointestinal disturbances). If fever occurs or the symptoms persist, other diagnoses need to be considered.
Treatment of Gorham's disease is for the most part palliative and limited to symptom management.
Sometimes the bone destruction spontaneously ceases and no treatment is required. But when the disease is progressive, aggressive intervention may be necessary. Duffy and colleagues reported that around 17% of patients with Gorham's disease in the ribs, shoulder, or upper spine experience extension of the disease into the chest, leading to chylothorax with its serious consequences, and that the mortality rate in this group can reach as high as 64% without surgical intervention.
A search of the medical literature reveals multiple case reports of interventions with varying rates of success as follows:
Cardiothoracic (heart & lung):
- Pleurodesis
- Ligation of thoracic duct
- Pleurperitoneal shunt
- Radiation therapy
- Pleurectomy
- Surgical resection
- Thalidomide
- Interferon alpha-2b
- TPN (total parenteral nutrition)
- Thoracentesis
- Diet rich in medium-chain triglycerides and protein
- Chemotherapy
- Sclerotherapy
- Transplantation
Skeletal:
- Interferon alpha-2b
- Bisphosphonate (e.g. pamidronate)
- Surgical resection
- Radiation therapy
- Sclerotherapy
- Percutaneous bone cement
- Bone graft
- Prosthesis
- Surgical stabilization
- Amputation
To date, there are no known interventions that are consistently effective for Gorham's and all reported interventions are considered experimental treatments, though many are routine for other conditions. Some patients may require a combination of these approaches. Unfortunately, some patients will not respond to any intervention.
A variety of methods may be used to treat the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans (of the hip joints). THRs are an effective means of treatment in the older population; however, in younger people they may wear out before the end of a person's life.
Other technicques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates which reduces the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN.
Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head. A 2012 Cochrane systematic review noted that no clear improvement can be found between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. More research is need to look into the effectiveness of hip core decompression for people with sickle cell disease.
Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique.
Osteomyelitis (OM) is an infection of bone. Symptoms may include pain in a specific bone with overlying redness, fever, and weakness. The long bones of the arms and legs are most commonly involved in children while the feet, spine, and hips are most commonly involved in adults.
The cause is usually a bacterial infection and rarely a fungal infection. It may occur via spread from the blood or from surrounding tissue. Risks for developing osteomyelitis include diabetes, intravenous drug use, prior removal of the spleen, and trauma to the area. Diagnosis is typically suspected based on symptoms. This is then supported by blood tests, medical imaging, or bone biopsy.
Treatment often involves both antimicrobials and surgery. In those with poor blood flow, amputation may be required. With treatment outcomes are often generally good when the condition has only been present a short time. About 2.4 per 100,000 people are affected a year. The young and old are more commonly affected. Males are more commonly affected than females. The condition was described at least as early as the 300s BC by Hippocrates. Before the availability of antibiotics the risk of death was significant.
The process is usually asymptomatic and benign, in which case the tooth does not require endodontic treatment.
The offending tooth should be tested for vitality of the pulp, if inflamed or necrotic, then endodontic treatment is required, while hopeless teeth should be extracted.
Treatment generally consists of surgical drainage, and long-term (6 to 8 weeks) use of antibiotics.
Treatment is usually symptomatic, (i.e., analgesic medications) and also the removal of debris from the socket by irrigation with saline or local anesthetic. Medicated dressings are also commonly placed in the socket; although these will act as a foreign body and prolong healing, they are usually needed due to the severe pain. Hence, the dressings are usually stopped once the pain is lessened. Examples of medicated dressings include antibacterials, topical anesthetics and obtundants, or combinations of all three, e.g., zinc oxide and eugenol impregnated cotton pellets, alvogyl (eugenol, iodoform and butamen), dentalone, bismuth subnitrate and iodoform paste (BIPP) on ribbon gauze and metronidazole and lidocaine ointment. A systematic review of the efficacy of treatments for dry socket concluded that there was not enough evidence to discern the effectiveness of any treatments. People who develop a dry socket typically seek medical/dental advice several times after the dental extraction, where the old dressing is removed, the socket irrigated and a new dressing placed. Curettage of the socket increases the pain and has been discouraged by some.
Pathologic fracture of the mandible is a possible complication of OM where the bone has been weakened significantly.
Supportive care must be provided to animals that have clinical signs. Subcutaneous or intravenous fluids are given to dehydrated animals, and severely anemic dogs may require a blood transfusion. Treatment for ehrlichiosis involves the use of antibiotics such as tetracycline or doxycycline for a period of at least six to eight weeks; response to the drugs may take one month. Treatment with macrolide antibiotics like clarithromycin and azithromycin is being studied. In addition, steroids may be indicated in severe cases in which the level of platelets is so low that the condition is life-threatening.
The prognosis is excellent, as no treatment is usually required.
If the offending tooth is extracted, the area of condensing osteitis may remain in the jaws indefinitely, which is termed osteosclerosis or bone scar.
A Cochrane review of low-intensity pulsed ultrasound to speed healing in newly broken bones found insufficient evidence to justify routine use. Other reviews have found tentative evidence of benefit. It may be an alternative to surgery for established nonunions.
Vitamin D supplements combined with additional calcium marginally reduces the risk of hip fractures and other types of fracture in older adults; however, vitamin D supplementation alone did not reduce the risk of fractures.
A systematic review reported that there is some evidence that rinsing with chlorhexidine (0.12% or 0.2%) or placing chlorhexidine gel (0.2%) in the sockets of extracted teeth reduces the frequency of dry socket. Another systematic review concluded that there is evidence that prophylactic antibiotics reduce the risk of dry socket (and infection and pain) following third molar extractions of wisdom teeth, however their use is associated with an increase in mild and transient adverse effects. The authors questioned whether treating 12 patients with antibiotics to prevent one infection would do more harm overall than good, in view of the potential side effects and also of antibiotic resistance. Nevertheless, there is evidence that in individuals who are at clear risk may benefit from antibiotics. There is also evidence that antifibrinolytic agents applied to the socket after the extraction may reduce the risk of dry socket.
Some dentists and oral surgeons routinely debride the bony walls of the socket to encourage hemorrhage (bleeding) in the belief that this reduces the incidence of dry socket, but there is no evidence to support this practice. It has been suggested that dental extractions in females taking oral contraceptives be scheduled on days without estrogen supplementation (typically days 23–28 of the menstrual cycle). It has also been suggested that teeth to be extracted be scaled prior to the procedure.
Prevention of alveolar osteitis can be exacted by following post-operative instructions, including:
1. Taking any recommended medications
2. Avoiding intake of hot fluids for one to two days. Hot fluids raise the local blood flow and thus interfere with organization of the clot. Therefore, cold fluids and foods are encouraged, which facilitate clot formation and prevent its disintegration.
3. Avoiding smoking. It reduces the blood supply, leading to tissue ischemia, reduced tissue perfusion and eventually higher incidence of painful socket.
4. Avoiding drinking through a straw or spitting forcefully as this creates a negative pressure within the oral cavity leading to an increased chance of blood clot instability.
External fixators can be used to prevent further damage to the leg until the patient is stable enough for surgery. It is most commonly used as a temporary measure. However, for some select cases it may be used as an alternative to intramedullary nailing for definitive treatment.
The first three cases of bisphosphonate-associated osteonecrosis of the jaw were spontaneously reported to the FDA by an oral surgeon in 2002, with the toxicity being described as a potentially late toxicity of chemotherapy. In 2003 and 2004, three oral surgeons independently reported to the FDA information on 104 cancer patients with bisphosphonate-associated osteonecrosis of the jaw seen in their referral practices in California, Florida, and New York. These case series were published as peer-reviewed articles — two in the "Journal of Oral and Maxillofacial Surgery" and one in the "Journal of Clinical Oncology". Subsequently, numerous instances of persons with this ADR were reported to the manufacturers and to the FDA. By December 2006, 3607 cases of people with this ADR had been reported to the FDA and 2227 cases had been reported to the manufacturer of intravenous bisphosphonates.
The International Myeloma Foundation's web-based survey included 1203 respondents, 904 patients with myeloma and 299 with breast cancer and an estimate that after 36 months, osteonecrosis of the jaw had been diagnosed in 10% of 211 patients on zoledronate and 4% of 413 on pamidronate. A population based study in Germany identified more than 300 cases of osteonecrosis of the jaw, 97% occurring in cancer patients (on high-dose intravenous bisphosphonates) and 3 cases in 780,000 patients with osteoporosis for an incidence of 0.00038%. Time to event ranged from 23–39 months and 42–46 months with high dose intravenous and oral bisphosphonates. A prospective, population based study by Mavrokokki "et al.". estimated an incidence of osteonecrosis of the jaw of 1.15% for intravenous bisphosphonates and 0.04% for oral bisphosphonates. Most cases (73%) were precipitated by dental extractions. In contrast, safety studies sponsored by the manufacturer reported bisphosphonate-associated osteonecrosis of the jaw rates that were much lower.
Although the majority of cases of ONJ have occurred in cancer patients receiving high dose intravenous bisphosphonates, almost 800 cases have been reported in oral bisphosphonate users for osteoporosis or Pagets disease. In terms of severity most cases of ONJ in oral bisphosphonate users are stage 1–2 and tend to progress to resolution with conservative measures such as oral chlorhexidine rinses.
Owing to prolonged embedding of bisphosphonate drugs in the bone tissues, the risk for BRONJ is high even after stopping the administration of the medication for several years.
This form of therapy has been shown to prevent loss of bone mineral density (BMD) as a result of a reduction in bone turnover. However, bone health entails quite a bit more than just BMD. There are many other factors to consider.
In healthy bone tissue there is a homeostasis between bone resorption and bone apposition. Diseased or damaged bone is resorbed through the osteoclasts mediated process while osteoblasts form new bone to replace it, thus maintaining healthy bone density. This process is commonly called remodelling.
However, osteoporosis is essentially the result of a lack of new bone formation in combination with bone resorption in reactive hyperemia, related to various causes and contributing factors, and bisphosphonates do not address these factors at all.
In 2011, a proposal incorporating both the reduced bone turnover and the infectious elements of previous theories has been put forward. It cites the impaired functionality of affected macrophages as the dominant factor in the development of ONJ.
In a systematic review of cases of bisphosphonate-associated ONJ up to 2006, it was concluded that the mandible is more commonly affected than the maxilla (2:1 ratio), and 60% of cases are preceded by a dental surgical procedure. According to Woo, Hellstein and Kalmar, oversuppression of bone turnover is probably the primary mechanism for the development of this form of ONJ, although there may be contributing co-morbid factors (as discussed elsewhere in this article). It is recommended that all sites of potential jaw infection should be eliminated before bisphosphonate therapy is initiated in these patients to reduce the necessity of subsequent dentoalveolar surgery. The degree of risk for osteonecrosis in patients taking oral bisphosphonates, such as alendronate (Fosamax), for osteoporosis is uncertain and warrants careful monitoring. Patients taking dexamethasone and other glucocorticoids are at increased risk.
Matrix metalloproteinase 2 may be a candidate gene for bisphosphonate-associated osteonecrosis of the jaw, since it is the only gene known to be associated with bone abnormalities and atrial fibrillation, both of which are side effects of bisphosphonates.