loader image

Global Regenerative Trade

MAGELLAN®

MAXILLO- FACIAL SURGERY

WHAT IS REGENERATIVE MEDICINE?

Regenerative Medicine encompasses many medical fields – Orthopedics and Spine Surgery, Sports Medicine, Gynecology, Urology, Oncology, Dermatology, Plastic surgery, Vascular Surgery, Cardiac surgery, etc.

Regenerative Medicine is the branch of medicine that develops methods to regrow, repair or replace damaged or diseased cells, organs or tissues. Regenerative medicine includes the generation and use of therapeutic stem cells, tissue engineering and the production of artificial organs. It uses autologous blood, bone marrow or adipose components to stimulate the body’s own repair processes. A common source for regenerative cells and growth factors are bone marrow aspirate concentrate (BMAC), platelet rich plasma (obtained from one’s own blood) and adipose derived stem cells.

PATHOLOGY

OSTEORADIONECROSIS OF THE MANDIBLE

Osteoradionecrosis (ORN) of the jaws, particularly of the mandible, is a long-term and serious complication of therapeutic radiotherapy for head and neck cancer. The mandible is affected more commonly than any other bones of the head and neck region. The incidence of ORN of mandible is reported to be between 2% and 22%. With the older radiation techniques, the rate of ORN was reported to be between 5% and 15%, whereas with newer techniques such as 3D conformal therapy and intensity modulated radiotherapy the rate of ORN has decreased to 6% or less. We here report a case of mandibular ORN and the literature review discusses the clinical features, pathogenesis, preventive measures, and management of ORN.

Osteoradionecrosis (ORN) describes the process where irradiated bone undergoes necrosis and becomes exposed through soft-tissue. The first report of ORN of the jaws after radiation therapy was published in 1992 by Regaurd. Ewing in 1926 first recognized and reported the bone changes associated with RT and described this disease state as radiation osteitis.

Radiation therapy in the head and neck cancer has a 20% chance of mandibular ORN. ORN is a late effect of radiotherapy. Early presentation within 2 years, is thought to be related to high dose of Radiation therapy (>70 gray), whereas late presentation is usually secondary to trauma and delayed wound healing with in compromised tissue.

Symptoms

Symptoms can vary depending on the grade or extent of the osteoradionecrosis and include:

  • pain
  • swelling
  • a sore, or ulcer, in the mouth or on the jaw
  • difficulty opening the jaw, or trismus
  • an abnormal opening, or fistula, between the jaw and the surface of the body
  • less feeling in the mouth or jaw, or even a complete loss of sensation in the area
  • infection
  • teeth that aren’t aligned properly, which is called malocclusion
  • jaw fracture not related to an accident or other trauma
  • exposed bone inside the mouth
  • bone sticking out through the skin, which is called sequestrum

Exposed bones and sequestrum are most often found under the jaw.

Report symptoms to your doctor or healthcare team as soon as possible.

JAW FRACTURE

A broken jaw (or mandible fracture) is a common facial injury. Only the nose is broken more frequently. A broken jaw is the 10th most common fractured bone in the human body. Fractures (breaks in the bone) are generally the result of a direct force or trauma to the jawbone (mandible).

A dislocated jawbone means that the temporomandibular joint (where the jaw connects with the skull) is moved out of place. The jawbone may or may not be fractured, but even if there is no fracture, symptoms (listed below) may be similar to a jawbone fracture. 

The jawbone, or mandible is the largest and main bone of the lower part of the face. Figure 1 shows the various anatomic regions of the mandible viewed from the right side. The anatomic region helps to classify the location of the fracture while the terms listed below describe the type of fracture:

  • Simple or closed: The fracture did not cause a break in the skin or mucosa or periodontal membrane. There is no connection between the jawbone and the environment.
  • Compound or open: The jawbone is open to the environment.
  • Comminuted: The jawbone region has bone splinters or crushed bone.
  • Greenstick: One section of the jawbone is fractured while the other part is bent.
  • Pathologic: fracture due to preexisting bone disease
  • Multiple: two or more distinct fractures of the jawbone
  • Impacted: One section of bone is driven by force into another section.
  • Atrophic: fracture due to bone atrophy
  • Indirect: fracture in a bone located away from the injury site
  • Complicated (complex): fracture with additional tissue or structural injury

     

    When to Seek Medical Care

    If after some trauma to the jaw or face, a person’s teeth don’t fit together correctly, if they have bleeding within the mouth, significant pain, problems speaking, or swelling, they should seek medical care.

    Broken jaw is best evaluated at a hospital. Therefore, most doctors will advise the person to go to an emergency department, preferably at a large hospital that would be more likely to have specialists (oral surgeons) on call to help evaluate and treat the individual if needed. A potential but serious consequence of jaw fractures is a problem breathing due to loss of support to the tongue. Therefore, any signs of breathing problems need to be addressed immediately by calling 911.

TEMPOROMANDIBULAR JOINT DYSFUNCTION

Temporomandibular joint dysfunction (TMDTMJD) is an umbrella term covering pain and dysfunction of the muscles of mastication (the muscles that move the jaw) and the temporomandibular joints (the joints which connect the mandible to the skull). The most important feature is pain, followed by restricted mandibular movement, and noises from the temporomandibular joints (TMJ) during jaw movement. Although TMD is not life-threatening, it can be detrimental to quality of life, because the symptoms can become chronic and difficult to manage.

Causes

TMD is a symptom complex (i.e. a group of symptoms occurring together and characterizing a particular disease), which is thought to be caused by multiple, poorly understood factors, but the exact etiology is unknown. There are factors which appear to predispose to TMD (genetic, hormonal, anatomical), factors which may precipitate it (trauma, occlusal changes, parafunction), and also factors which may prolong it (stress and again parafunction). Overall, two hypotheses have dominated research into the causes of TMD, namely a psychosocial model and a theory of occlusal dysharmony. Interest in occlusal factors as a causative factor in TMD was especially widespread in the past, and the theory has since fallen out of favor and become controversial due to lack of evidence.

Disc displacement

In people with TMD, it has been shown that the lower head of lateral pterygoid contracts during mouth closing (when it should relax), and is often tender to palpation. To theorize upon this observation, some have suggested that due to a tear in the back of the joint capsule, the articular disc may be displaced forwards (anterior disc displacement), stopping the upper head of lateral pterygoid from acting to stabilize the disc as it would do normally. As a biologic compensatory mechanism, the lower head tries to fill this role, hence the abnormal muscle activity during mouth closure. There is some evidence that anterior disc displacement is present in proportion of TMD cases. Anterior disc displacement with reduction refers to abnormal forward movement of the disc during opening which reduces upon closing. Anterior disc displacement without reduction refers to an abnormal forward, bunched-up position of the articular disc which does not reduce. In this latter scenario, the disc is not intermediary between the condyle and the articular fossa as it should be, and hence the articular surfaces of the bones themselves are exposed to a greater degree of wear (which may predispose to osteoarthritis in later life).

Degenerative joint disease

The general term “degenerative joint disease” refers to arthritis (both osteoarthritis and rheumatoid arthritis) and arthrosis. The term arthrosis may cause confusion since in the specialized TMD literature it means something slightly different from in the wider medical literature. In medicine generally, arthrosis can be a nonspecific term for a joint, any disease of a joint (or specifically degenerative joint disease), and is also used as a synonym for osteoarthritis. In the specialized literature that has evolved around TMD research, arthrosis is differentiated from arthritis by the presence of low and no inflammation respectively. Both are however equally degenerative. The TMJs are sometimes described as one of the most used joints in the body. Over time, either with normal use or with parafunctional use of the joint, wear and degeneration can occur, termed osteoarthritis. Rheumatoid arthritis, an autoimmune joint disease, can also affect the TMJs. Degenerative joint diseases may lead to defects in the shape of the tissues of the joint, limitation of function (e.g. restricted mandibular movements), and joint pain.

Psychosocial factors

Emotional stress (anxiety, depression, anger) may increase pain by causing autonomic, visceral and skeletal activity and by reduced inhibition via the descending pathways of the limbic system. The interactions of these biological systems have been described as a vicious “anxiety-pain-tension” cycle which is thought to be frequently involved in TMD. Put simply, stress and anxiety cause grinding of teeth and sustained muscular contraction in the face. This produces pain which causes further anxiety which in turn causes prolonged muscular spasm at trigger points, vasoconstriction, ischemia and release of pain mediators. The pain discourages use of the masticatory system (a similar phenomenon in other chronic pain conditions is termed “fear avoidance” behavior), which leads to reduced muscle flexibility, tone, strength and endurance. This manifests as limited mouth opening and a sensation that the teeth are not fitting properly.

Persons with TMD have a higher prevalence of psychological disorders than people without TMD. People with TMD have been shown to have higher levels of anxiety, depression, somatization and sleep deprivation, and these could be considered important risk factors for the development of TMD. In the 6 months before the onset, 50–70% of people with TMD report experiencing stressful life events (e.g. involving work, money, health or relationship loss). It has been postulated that such events induce anxiety and cause increased jaw muscle activity. Muscular hyperactivity has also been shown in people with TMD whilst taking examinations or watching horror films.

Others argue that a link between muscular hyperactivity and TMD has not been convincingly demonstrated, and that emotional distress may be more of a consequence of pain rather than a cause.

Bruxism

Bruxism is an oral parafunctional activity where there is excessive clenching and grinding of the teeth. It can occur during sleep or whilst awake. The cause of bruxism itself is not completely understood, but psychosocial factors appear to be implicated in awake bruxism and dopaminergic dysfunction and other central nervous system mechanisms may be involved in sleep bruxism. If TMD pain and limitation of mandibular movement are greatest upon waking, and then slowly resolve throughout the day, this may indicate sleep bruxism. Conversely, awake bruxism tends to cause symptoms that slowly get worse throughout the day, and there may be no pain at all upon waking.

The relationship of bruxism with TMD is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. Indeed, the symptoms of TMD overlap with those of bruxism. Others suggest that there is no strong association between TMD and bruxism. A systematic review investigating the possible relationship concluded that when self-reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when more strict diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. Self-reported bruxism is probably a poor method of identifying bruxism. There are also very many people who grind their teeth and who do not develop TMD. Bruxism and other parafunctional activities may play a role in perpetuating symptoms in some cases.

Other parafunctional habits such as pen chewing, lip and cheek biting (which may manifest as morsicatio buccarum or linea alba), are also suggested to contribute to the development of TMD. Other parafunctional activities might include jaw thrusting, excessive gum chewing, nail biting and eating very hard foods.

PROCEDURES

SINUS AUGMENTATION

Maxillary sinus floor augmentation (also termed sinus liftsinus graftsinus augmentation or sinus procedure) is a surgical procedure which aims to increase the amount of bone in the posterior maxilla (upper jaw bone), in the area of the premolar and molar teeth, by lifting the lower Schneiderian membrane (sinus membrane) and placing a bone graft.

When a tooth is lost the alveolar process begins to remodel. The vacant tooth socket collapses as it heals leaving an edentulous (toothless) area, termed a ridge. This collapse causes a loss in both height and width of the surrounding bone. In addition, when a maxillary molar or premolar is lost, the maxillary sinus pneumatizes in this region which further diminishes the thickness of the underlying bone. Overall, this leads to a loss in volume of bone that is available for implantation of dental implants, which rely on osseointegration (bone integration), to replace missing teeth. The goal of the sinus lift is to graft extra bone into the maxillary sinus, so more bone is available to support a dental implant.

Indications

While there may be a number of reasons for wanting a greater volume of bone in the posterior maxilla, the most common reason in contemporary dental treatment planning is to prepare the site for the future placement of dental implants.

Sinus augmentation (sinus lift) is performed when the floor of the sinus is too close to an area where dental implants are to be placed. This procedure is performed to ensure a secure place for the implants while protecting the sinus. Lowering of the sinus can be caused by: Long-term tooth loss without the required treatment, periodontal disease, trauma.

Patients who have the following may be good candidates for sinus augmentation.

  • Lost more than one tooth in the posterior maxilla.
  • Lost a significant amount of bone in the posterior maxilla.
  • Missing teeth due to genetics or birth defect.
  • Minus most of the maxillary teeth and need a strong sinus floor for multiple implants.

It is not known if using sinus lift techniques is more successful than using short implants for reducing the number of artificial teeth or dental implant failures up to a year after teeth/implant placement.

SUPPORTING EVIDENCE

MANDIBLE

MAXILLA

SINUS AUGMENTATION

TEMPOROMANDIBULAR JOINT

VIDEOS

Vivostat Logo

THE VIVOSTAT® SYSTEM

The uniqueness of the Vivostat® system is a novel patented biotechnological process that enables reliable and reproducible preparation of autologous Fibrin Sealant or Platelet Rich Fibrin (PRF®) without using cryoprecipitation and without the need for a separate thrombin component.

THE FULLY AUTOMATED VIVOSTAT® SYSTEM CONSISTS OF THREE COMPONENTS:

  • The Processor Unit is a non-sterile, reusable, fully automated device that controls the biochemical process.
  • The Processor Unit is used to process the patient’s blood and prepare the Vivostat® Fibrin Sealant or Vivostat PRF® solution.
Vivostat Processor Product
  • The Processor Unit is operated by a single button and a display keeps the nurse informed of the remaining process time and status at all times. No specific installation is required and the large wheelbase makes moving it easy.
  • The Processor Unit can be located in any room or corridor in the operating department. It is most often placed centrally between the operating theatres. This way one Processor Unit can supply a number of operating theatres.
  • In approx.  25 min a concentrated fibrin sealant or PRF® solution is prepared from the patient’s whole blood.
  • The Applicator Unit is a non-sterile, reusable, fully automated device that controls the delivery of the Vivostat® Fibrin Sealant or Vivostat PRF®.
Vivostat Processor Product
  • The large display and integrated microprocessor automatically primes the Spraypen® and informs the surgeon of the remaining volume of fibrin sealant/PRF® throughout the entire process.
  • Different spray modes can be selected depending on the actual procedure or area to be covered. Like the Processor Unit it has a large wheelbase and can easily be moved if required.
  • The disposable set comprises of two parts: A Preparation Kit used to prepare the fibrin sealant or PRF® solution before surgery, and an Application Kit used to activate and apply the fibrin sealant/PRF® solution.

 

  • Preparation Kit
    The Preparation Kit contains the specially designed Preparation Unit – a sterile disposable device in which the patient’s blood is collected, the biochemical process carried out, and the fibrin sealant or PRF® solution harvested.

 

  • The Application Kit
    The Application Kit contains the Spraypen®1 and all other items required to prepare the system for the delivery of the fibrin sealant or PRF® solution. The Spraypen® is a sterile, disposable, hand held device which delivers the fibrin sealant or PRF® solution to the tissue. The revolutionary and patented design offers the surgeon unparalleled freedom in controlling the application unlike any other product on the market today.

 

1Besides the Spraypen®, the Vivostat® system offers different types of applicators, e.g. the Endoscopic Applicator. For a full list of application devices click here

1-2-3 Spray

Three easy steps to prepare Vivostat® Fibrin Sealant or Vivostat PRF®

1. Draw blood from the Patient

Fibrin Prep With Blood Inside

At the time of surgery or up to 24 hours before1, citrate (supplied with the kit) is added to the Preparation Unit. 120 ml of the patient’s own blood is then drawn into the same unit.

2. Process the patient’s blood

Vivostat Processor 800

The Preparation Unit is placed in the Processor Unit. At the touch of a button the process starts; after approx. 25 minutes, an autologous fibrin or PRF® solution is ready for use. No thrombin or bovine components are added to the blood at any time.

3. Load the Applicator Unit and spray

Vivostat Display Applicator

The Fibrin or PRF® solution is easily loaded into the Applicator Unit and applied to the surgical site using one of the unique application devices (e.g. the Spraypen). 1This depends on the type of kit being used. Always consult the “Instructions for Use” supplied with the kit to determine the correct preparation.

The following video illustrates how to prepare and apply autologous fibrin sealant.

Presentation DVD from Vivostat A/S on Vimeo.