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Recovery from renal osteodystrophy has been observed following kidney transplantation. Renal osteodystrophy is a chronic condition with a conventional hemodialysis schedule. Nevertheless, it is important to consider that the broader concept of CKD-MBD, which includes renal osteodystrophy, is not only associated with bone disease and increased risk of fractures but also with cardiovascular calcification, poor quality of life and increased morbidity and mortality in CKD patients (the so-called bone-vascular axis). Actually, bone may now be considered a new endocrine organ at the heart of CKD-MBD.
Treatment for renal osteodystrophy includes the following:
- calcium and/or native vitamin D supplementation
- restriction of dietary phosphate (especially inorganic phosphate contained in additives)
- phosphate binders such as calcium carbonate, calcium acetate, sevelamer hydrochloride or carbonate, lanthanum carbonate, sucroferric oxyhydroxide, ferric citrate among others
- active forms of vitamin D (calcitriol, alfacalcidol, paricalcitol, maxacalcitol, doxercalciferol, among others)
- cinacalcet
- renal transplantation
- haemodialysis five times a week is thought to be of benefit
- parathyroidectomy for symptomatic medication refractive end stage disease
Although the exact cause of Panner Disease is unknown, in recent research, it has been concluded that it may be associated with frequent throwing or other athletic activity. In the same article that talks about varying osteochondrosis diseases, it is pointed out that Panner Disease always involves alteration of the capitellum, which can be visualized by radiography. In another research article, the research team aimed to summarize the best available evidence for diagnosis and treatment for Panner Disease. In the article it was found that the most common symptoms that patients with Panner Disease present with are elbow stiffness and swelling, limited range of motion, and limited elbow extension. In alignment with the previously mentioned article, the team of researchers also concluded that Panner Disease involves irregularity of the capitellum, specifically that it appears flattened. Panner Disease often gets misdiagnosed as osteochondritis dissecans (OCD), and in this article they distinguish the difference between the two diseases are age difference and radiographic findings. In alignment with the two previously discussed articles, another article that reports on three case studies of Panner Disease, states that the primary treatment that is used for Panner Disease is rest and restriction from all physical and athletic activity that involves the use of the upper extremities; the activity is suggested to be ceased until the symptoms are relieved.
If the ringbone is close to a joint, the prognosis for the horse's continued athletic use is not as good as if the ringbone is not near a joint. Ringbone that is progressing rapidly has a poorer prognosis as well.
Horses that are not performing strenuous work, such as jumping or working at speed, will probably be usable for years to come. However, horses competing in intense sports may not be able to continue at their previous level, as their pastern joints are constantly stressed.
Treatment options include modified activity with or without weight bearing; immobilization; cryotherapy; anti-inflammatory medication; drilling of subchondral bone; microfracture; removal or reattachment of loose bodies; mosaicplasty and osteoarticular transfer system (OATS) procedures. The primary goals of treatment are:
1. Enhance the healing potential of subchondral bone;
2. Fix unstable fragments while maintaining joint congruity; and
3. Replace damaged bone and cartilage with implanted tissues or cells that can grow cartilage.
The articular cartilage's capacity for repair is limited: partial-thickness defects in the articular cartilage do not heal spontaneously, and injuries of the articular cartilage which fail to penetrate subchondral bone tend to lead to deterioration of the articular surface. As a result, surgery is often required in even moderate cases where the osteochondral fragment has not detached from the bone (Anderson Stage II, III).
The choice of surgical versus non-surgical treatments for osteochondritis dissecans is controversial. Consequently, the type and extent of surgery necessary varies based on patient age, severity of the lesion, and personal bias of the treating surgeon—entailing an exhaustive list of suggested treatments. A variety of surgical options exist for the treatment of persistently symptomatic, intact, partially detached, and completely detached OCD lesions. Post-surgery reparative cartilage is inferior to healthy hyaline cartilage in glycosaminoglycan concentration, histological, and immunohistochemical appearance. As a result, surgery is often avoided if non-operative treatment is viable.
A recent article in 2015 reported a persistent notochord in a fetus at 23 weeks of gestation. The fetus had an abnormal spine, shortened long bones and a left clubfoot. After running postmortem tests and ultrasound, the researchers believed that the fetus suffered from hypochondrogenesis. Hypochondrogenesis is caused when type II collagen is abnormally formed due to a mutation in the COL2A1 gene. Normally, the cartilaginous notochord develops into the bony vertebrae in a human body. The COL2A1 gene results in malformed type II collagen, which is essential in the transition from collagen to bone. This is the first time that researchers found a persistent notochord in a human body due to a COL2A1 mutation.
Like treatment options, the prognosis is dependent on the severity of the symptoms. Despite the various symptoms and limitations, most individuals have normal intelligence and can lead a normal life.
The goal of treatment in Panner disease is to relieve pain. Treatment for Panner Disease is very minimal because in most children the bones repair their blood supply and rebuild themselves and this leads to the rebuilding of the growth plate and the capitellum returns to its normal shape. The period of rebuilding and regrowth varies from child to child and can last anywhere between weeks to several months. To relieve the pain, the child is restricted from participating in sports and activities until the elbow is healed and to also rest the affected elbow. Rest will allow for the pain to be relieved and return of full elbow movement. It may also be recommended for children to apply an icepack or heat to the elbow to alleviate pain and swelling. If the child has great difficulty bending and straightening the arm then physical therapy may also be recommend. Occasionally, it is recommended for children to use nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen to also reduce pain and swelling. For treatment, Panner Disease heals well in children with rest and restriction of physical activity and sports using the affected arm. The prognosis is also good with treatment and the affected capitellum is remodeled. Irregularities of the capitellum and surrounding elbow area can both be seen by radiograph and MRI. When treatment is effective the flattened and fragmented capitellum is completely remodeled and returns to its normal circular shape, and also the high intensity signal on a MRI T2 series disappears. These results indicate that the capitellum is completely remodeled and the child is able to return to normal physical and sports activities.
Simple (Unicameral) Bone Cyst
Some unicameral bone cysts may spontaneously resolve without medical intervention. Specific treatments are determined based on size of the cyst, strength of the bone, medical history, extent of the disease, activity level, symptoms an individual is experiencing, and tolerance for specific medications, procedures, or therapies. The types of methods used to treat this type of cyst are curettage and bone grafting, aspiration, steroid injections, and bone marrow injections. Watchful waiting and activity modifications are the most common nonsurgical treatments that will help resolve and help prevent unicameral bone cysts from occurring and reoccurring.
Aneurysmal Bone Cyst
The aneurysmal bone cyst can be treated with a variety of different methods. These methods include open curettage and bone grafting with or without adjuvant therapy, cryotheraphy, sclerotherapy, ethibloc injections, radionuclide ablation, and selective arterial embolization. En-block resection and reconstruction with strut grafting are the most common treatments and procedures that prevent recurrences of this type of cyst.
Traumatic Bone Cyst
The traumatic bone cyst treatment consists of surgical exploration, curettage of the osseous socket and bony walls, subsequent filling with blood, and intralesional steroid injections. Young athletes can reduce their risk of traumatic bone cyst by wearing protective mouth wear or protective head gear.
Ringbone is degenerative (unless it is caused by direct trauma). Treatment works to slow down the progress of the bony changes and alleviate the horse's pain, rather than working to cure it.
Shoeing: The farrier should balance the hoof and apply a shoe that supports the heels and allows for an easy breakover.
NSAIDs: or non-steroidal anti-inflammatory drugs help to alleviate the pain and reduce inflammation within and around the joints. Often NSAIDs make the horse comfortable enough to continue ridden work, which is good for the horse's overall health.
Joint injections: The pastern joint can be injected directly, typically with a form of corticosteroid and hyaluronic acid.
Extracorporeal shockwave therapy: A high intensity specialized percussion device can help to remodel new bone tissue and decrease pain.
Arthrodesis: the fusion of the two bones of the pastern joints eliminates the instability of the joint, and thus the inflammation. This procedure may then eliminate the horse's lameness as well. However, surgical alteration of the joint can promote the growth of bone in the area, which is cosmetically displeasing. Arthrodesis of the coffin joint is usually not performed due to the location of the joint (within the hoof) and because the coffin joint needs some mobility for the horse to move correctly (unlike the pastern joint, which is very still).
Interleukin-1 receptor antagonist protein (IRAP) blocks IL-1 from binding to tissues and inhibits the damaging consequences of IL-1.
Microcurrent technology: Tissue, including muscle, tendons, ligaments, skin and bone, is formed from a large mass of similar cells that perform specific functions. These cells use tiny sequences of electric current, measured in millionths of an amp, to organise, monitor and regulate a stable state within the body.
When there is injury, damage or disease to a tissue, there is disruption to the normal electrical current within the cells and things fail to work properly. By introducing the correct sequences the body's natural electric circuitry is replicated and kick starts and accelerates normal functioning.
Preventive maintenance therapy for the oral effects of TDO involve frequent dental cleanings, professional application of desensitizing medication, diet counseling, and oral hygiene instructions in proper home care and maintenance; medicated dental rinses and toothpastes are also prescribed as people suffering from TDO are more prone to oral hard tissue disease and early tooth loss. If restorative dentistry is performed without orthodontics to correct the protrusion of the lower jaw, a dental night guard worn at bedtimes on the upper or lower teeth to protect them from the effects of grinding may be recommended.
In extreme cases, tooth loss is inevitable, and the patient will consult with a prosthodontist to determine tooth replacement options such as dental implants, or partial dentures. There is no cure for TDO, but managing its oral and systemic affects is key to having the most favorable outcome from the disease. As the person affected by TDO ages, increased bone fractures may occur. The person suffering from TDO should watch for any pimple like masses on the gum tissue, pain or soreness in the teeth and gums, broken or chipped teeth, feeling of water in the ear or severe pain in the extremities which could indicate fracture.
A bone cyst or geode is a cyst that forms in bone.
Types include:
- Unicameral bone cyst
- Aneurysmal bone cyst
- Traumatic bone cyst
The hair, teeth, and skeletal side effects of TDO are lifelong, and treatment is used to manage those effects. A person with TDO has the same life expectancy as a person without TDO. There are no cures or medications used to treat systemic effects of TDO, but medications for the frequent ear and dental infections can be used to manage its symptoms. A team based approach between dental specialists, oral and maxillofacial surgeons, and physicians is necessary for treating the systemic effects and improves the prognosis. It is also recommended for affected individuals to seek counseling to be better able to cope with any psychosocial problems due to oral and facial abnormalities that occur with TDO.
At home, a person suffering from TDO may be instructed to use frequent deep conditioning treatments and low manipulation hair styling to control shedding and hair loss. Clinical treatment involves the use of radiology to determine the effects that TDO has had on the surrounding teeth and bone structures. A series of appointments with the healthcare team are usually necessary to correct TDO abnormalities with treatment duration lasting from several months to through full oral-facial maturation stages.
Endodontic procedures are routinely recommended due to treatdental pulp exposure or periodontal abscess. Maxillofacial surgery may be required to establish a more appropriate mastication, skeletal, and esthetic relationship vertically between the teeth to improve functioning. Esthetic procedures such as dental crown (dentistry) or veneer (dentistry) are often performed to improve the physical look of the teeth and to strengthen the weak enamel caused by TDO.
Management of this condition includes|:
- Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow.
- However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)-D, i.e. calcitriol) are often necessary to prevent further decline
Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.
There is currently no cure for GAPO syndrome, but some options are available to reduce the symptoms. Nearsightedness, which affects some sufferers of the disease, can be treated by corrective lenses. Unfortunately, optic atrophy as a result of degradation of the optic nerve (common with GAPO syndrome) cannot be corrected. Corticosteroids have been proposed as a treatment for optic nerve atrophy, but their effectiveness is disputed, and no steroid based treatments are currently available.
Like all fractures, consideration has to be given to other illnesses that might jeopardize the patient, then to reduction and fixation of the fracture itself. Except in avulsive type injuries, or those where there might be airway compromise, a several day delay in the treatment of mandible fractures seems to have little impact on the outcome or complication rates.
Treatment is aimed at achieving a stable, aligned, mobile and painless joint and to minimize the risk of post-traumatic osteoarthritis. To achieve this operative or non-operative treatment plans are considered by physicians based on criteria such as patient characteristics, severity, risk of complications, fracture depression and displacement, degree of injury to ligaments and menisci, vascular and neurological compromise.
For early management, traction should be performed early in ward. It can either be Skin Traction or Skeletal Traction. Depends on the body weight of patient and stability of the joint. Schantz pin insertion over the Calcaneum should be done from Medial to lateral side.
Later when condition is stable. Definitive plan would be Buttress Plating and Lag Screw fixation.
In some cases, surgery is the only way to eliminate or reduce pain. There are several types of surgery for treatment of hallux rigidus. The type of surgery is based on the stage of hallux rigidus.
Supracondylar humerus fractures account for 55%-75% of all elbow fractures. They most commonly occur in children between ages 5–8, because remodeling of bone in this age group causes a decreased supracondylar anteroposterior diameter.
X-linked SCID is a known pediatric emergency which primarily affects males. If the appropriate treatment such as intravenous immunoglobulin supplements, medications for treating infections or a bone marrow transplant is not administered, then the prognosis is poor. The patients with X-linked SCID usually die two years after they are born. For this reason, the diagnosis of X-linked SCID needs to be done early to prevent any pathogens from infecting the infant.
However, the patients have a higher chance of survival if the diagnosis of X-linked SCID is done as soon as the baby is born. This involves taking preventative measures to avoid any infections that can cause death. For example, David Vetter had a high chance of having X-linked SCID because his elder sibling had died due to SCID. This allowed the doctors to place David in the bubble and prevented infections. In addition, if X-linked SCID is known to affect a child, then live vaccines should not be administered and this can save the infants life. Vaccines, which are pathogens inserted into the body to create an immune response, can lead to death in infants with X-linked SCID. Moreover, with proper treatments, such as a bone marrow transplant, the prognosis is good. The bone marrow transplant has been successful in treating several patients and resulted in a full immune reconstitution and the patient can live a healthy life. The results of bone marrow transplant are most successful when the closest human leukocyte antigen match has been found. If a close match is not found, however, there is a chance of graft-versus-host-disease which means the donor bone marrow attacks the patient's body. Hence, a close match is required to prevent any complications.
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers,reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.
Stage 3 hallux rigidus often involves significant cartilage loss and may be treated by an osteotomy in which cartilage on the first metatarsal head is repositioned, possibly coupled with a hemi-implant in which the base of the proximal phalanx (base of the big toe) is resurfaced.
Tibial plateau fractures constitute 1% of all fractures. Peak age is 30–40 years old in men and 60-70 in women. Approximately half of the people who sustain a tibial plateau fracture are aged over 50 years old.