Leukemia and its treatment

General Considerations regarding Leukemia

 

Leukemia is a malignant disease of the blood, where the uncontrolled proliferation of immature blood cells that originate from hematopoietic stem cell mutation occurs. Eventually these aberrant cells compete with normal cells for space in the bone marrow, causing bone marrow failure and death.

 

Classification of leukemia

The most common leukemias are generally classified as

  1. Acute lymphocytic
  2. Acute myeloid
  3. Chronic lymphocytic
  4. Chronic myeloid

The classification criteria of leukemia is histological and is based on

  1. The similarity between the leukemic cells and normal cells (myeloid versus lymphoid) and
  2. The clinical course of the disease (acute versus chronic).

The acute forms of leukemia result from the accumulation of immature and functionless cells in the bone marrow, with rapid progression, rapidly fatal in untreated patients. Chronic leukemias, in turn, begin slowly with uncontrolled proliferation of more mature and differentiated cells.

 

Treatment of leukemia

The treatment of leukemia depends on factors such as type and subtype of the disease, risk factors, and age of the patient.

Generally, the recommended treatment is chemotherapy with or without adjuvant treatments.

Hematopoietic stem cell transplantation (HSCT) is also done as mentioned below:


1.
Acute lymphoblastic leukemia (ALL):

  • Prophase (initial reduction of leukemic cells),
  • Induction (achieve complete remission),
  • Consolidation (increase the quality of remission),
  • Intensification (post-remission further reduction), and
  • Maintenance therapy (maintenance of consolidation)
  • Prophylactic central nervous system (CNS) therapeutic irradiation or irradiation if CNS is involved;
  • The HSCT can be done in some cases

2. Acute myeloid leukemia (AML):

  • Induction (until complete remission)
  • Consolidation
  • Intensification

3. Chronic myeloid leukemia (CML):

  • Remission of leukemic cells and Philadelphia chromosome-positive with high doses of chemotherapy, monitoring of therapy, and HSCT

4. Chronic lymphocytic leukemia (CLL):

  • Conventional treatment is not curative; chemotherapy is performed as a control.

 

Special Considerations about HSCT

Treatment with HSCT aims to repopulate the marrow with normal healthy cells which were earlier destroyed with high doses of chemotherapy with or without radiation.

The HSCT can be of the autologous type (patient's own hematopoietic stem cells) or allogeneic (hematopoietic cells obtained from a donor) and consists of five phases:

  1. Preconditioning
  2. Neutropenic phase conditioning
  3. Engraftment to hematopoietic recovery
  4. Immune reconstitution/recovery from systemic toxicity
  5. Long-term survival.

The main complications of HSCT are graft rejection (for failure in the patient's immunosuppression) and the graft-versus-host disease (GVHD), where immunocompetent donor cells attack the patient's antigens, which may lead to the depletion of T lymphocytes. Potentially fatal, GVHD can occur soon after HSCT (acute GVHD) or after a few months (chronic GVHD or cGVHD). With deep and long immunosuppression, the patient becomes susceptible to fungal and viral infections.

 

Oral Manifestations of Leukemia

Special considerations regarding oral complications, oral health, and dental treatment in Hemopoetic Stem Cell Transplantation

 

 

 

 

 

 

 

 

 

Referrence: Caroline Zimmermann, Maria Inês Meurer, Liliane Janete Grando, Joanita Ângela Gonzaga Del Moral, Inês Beatriz da Silva Rath, and Silvia Schaefer Tavares Journal of Oncology Volume 2015 (2015), Article ID 571739, 14 pages http://dx.doi.org/10.1155/2015/571739

Oral Manifestations of Leukemia

The oral manifestation of leukemia can be summarized as follows.

In acute leukemias localized or generalized gingival hyperplasia is generally observed.

It mainly affects the interdental papillae and the marginal gingiva.

It is caused by inflammation, or leukemic infiltration, and may be localized or generalized, the latter being the most common form.

The infiltration of leukemic cells may also involve periapical tissues and simulate, both clinically and radiographically, periapical inflammatory lesions.

In chronic leukemia, the leukemic infiltrates in oral tissues is less frequent and can be observed:

  1. Pallor of the mucosa
  2. Soft tissue infections
  3. Generalized lymphadenopathy

The manifestations of thrombocytopenia are more common when the platelet count is below 50,000 cells/mm3 and may manifest as bruising, petechiae in the hard and soft palate, and also spontaneous gingival bleeding, especially if the platelet count is below 20,000 cells/mm3.

Opportunistic infections with Candida albicans and Herpes viruses are common and can involve any area of the mucosa. Ulcers can also result from impaired immune defense in combating normal microbial flora.

Oral Manifestations Related to Hematopoietic stem cell transplantation (HSCT)

The most common oral manifestations related to pre-, immediate post-, and late post-HSCT are summarized in Table 1.

The oral manifestations that may be present are correlated with the phases of HSCT:

  1. Preconditioning: oral infections, ulceration, bleeding, and temporomandibular joint dysfunction;
  2. Neutropenic phase conditioning: mucositis, dysgeusia, xerostomia, bleeding, oral pain, opportunistic infections, neurotoxicity, and temporomandibular dysfunction, usually manifesting with high prevalence and severe forms; at this stage, the patient may develop hyperacute GVHD with further severe oral complications;
  3. Engraftment to hematopoietic recovery: opportunistic infections are common and acute GVHD becomes a concern; bleeding may be present, xerostomia, neurotoxicity, granulomas/papillomas, and temporomandibular dysfunction;
  4. Immune reconstitution/recovery from systemic toxicity: salivary dysfunction, late viral infections, craniofacial growth abnormalities, cGVHD, and squamous cell carcinoma; and
  5. The long-term survival: in pediatric patients, particularly children under 6 years, one can observe complications in the development of bones and teeth; at this stage, recurrence and malignant neoplasms can be observed.
  6. In the occurrence of GVHD, mucositis, gingivitis, erythema, and pain are usually observed.

In cGVHD, the most common oral manifestations are lichen-type features, hyperkeratotic plaques, mucocele, atrophic mucosa, ulceration, fibrosis with limited mouth opening, hyposalivation, and xerostomia,In addition, secondary to cGVHD, the patients have a greater tendency to develop malignancies.

 

Leukemia and its treatment

Special considerations regarding oral complications, oral health, and dental treatment in Hemopoetic Stem Cell Transplantation

 

 

 

Reference: Caroline Zimmermann, Maria Inês Meurer, Liliane Janete Grando, Joanita Ângela Gonzaga Del Moral, Inês Beatriz da Silva Rath, and Silvia Schaefer Tavares Journal of Oncology Volume 2015 (2015), Article ID 571739, 14 pages http://dx.doi.org/10.1155/2015/571739

Special considerations regarding oral complications, oral health, and dental treatment in Hemopoetic Stem Cell Transplantation

Table 1: Special considerations regarding oral complications, oral health, and dental treatment in pre-, immediate post-, and late post-HSCT.

Special considerations Pre-HSCT
(preconditioning)
Immediate post-HSCT
(neutropenic conditioning phase and engraftment to hematopoietic recovery)
Late post-HCST
(immune reconstitution/recovery from systemic toxicity and long-term survival)
Oral manifestations (i) Oral infections
(ii) Soreness
(iii) Bleeding
(iv) Temporomandibular dysfunction.
(i) Mucositis
(ii) Dysgeusia
(iii) Xerostomia
(iv) Hemorrhage
(v) Oral pain
(vi) Opportunistic infections
(vii) Neurotoxicity
(viii) Temporomandibular dysfunction
(ix) Acute GVHD.
(i) Chronic GVHD
(ii) Late viral infections
(iii) Salivary dysfunction
(iv) Squamous cell carcinoma
(v) Craniofacial growth abnormalities (children)
(vi) Impairment of bones and teeth (children).
Oral health (i) Identify and eliminate sources of existing or potential infection.
(ii) Orientate the patient about the importance of maintaining oral health.
(iii) Warn about the possible effects of antineoplastic therapy in the oral cavity.
(i) Maintain and reinforce the importance of optimal oral health.
(ii) Treat side effects of HSCT therapy.
(iii) Pay attention to periodontitis and gingivitis as potential sources of bacteremia.
(i) Diagnosis and treatment of mucosal lesions and lichen-type features with symptoms
(ii) Caries prevention and reestablishment of oral health in case of rampant caries
(iii) Treatment of hyposalivation and xerostomia
(iv) Early detection of oral cancer and precursor lesions.
Dental treatment (i) Complete necessary dental treatment
(ii) Elective treatment should be delayed until the re-establishment of immunity (at least 100 days after transplant, or more in the case of oral complications or other cGVHD).
Neutropenic conditioning phase
(i) Dental procedures should not be performed at this stage
(ii) If emergencies, perform the necessary dental approach, with the participation of medical staff.
Engraftment to hematopoietic recovery
(i) Monitoring and management of oral complications of HSCT
(ii) Invasive procedures only with the approval of the medical team
(iii) Strengthening the maintenance guidelines of good oral hygiene and noncariogenic diet
(iv) Special attention to xerostomia and GVHD.
Immune reconstitution/recovery from systemic toxicity
(i) Periodic dental evaluation
(ii) Avoid invasive procedures
(iii) Clarify risks and benefits of orthodontic appliances.
Long-term survival
(i) Periodic dental evaluation
(ii) In the first 12 months after HSCT:
(a) avoid routine dental care, including scaling and periodontal planning;
(b) if emergencies, strategies to reduce inhalation of aerosols and antibiotic prophylaxis;
(c) before invasive procedures, consider the use of IgG, antibiotics, corticosteroids, and/or platelet transfusion.

Leukemia and its treatment

Oral Manifestations of Leukemia

Referrence: Caroline Zimmermann, Maria Inês Meurer, Liliane Janete Grando, Joanita Ângela Gonzaga Del Moral, Inês Beatriz da Silva Rath, and Silvia Schaefer Tavares Journal of Oncology Volume 2015 (2015), Article ID 571739, 14 pages http://dx.doi.org/10.1155/2015/571739

Effect of diabetes on osseointegration and dental implants

The tenacious hyperglycemia in diabetic people, hinder osteoblastic activity and modifies the response of parathyroid hormone that adjusts metabolism of Ca and P, decreases collagen synthesis during callus formation, induces apoptosis in lining cells of bone and increases osteoclastic activity due to untiring inflammatory response. It also stimulates deleterious effect on bone matrix and reduces growth and buildup of extracellular matrix. The subsequent result is reduced bone formation during healing.

Type -1 diabetes (insulin dependent) causes decreased bone formation, as well as reduced bone mineral density and higher bone resorption while Type -2 diabetes (non-insulin dependent) produces normal or greater bone mineral density in some patients. It has been detected that insulin not only diminishes the harmful effect of hyperglycemia by controlling it but also stimulates osteoblastic activity.

Success/failure of dental implants in diabetic patients

Most of the studies detected slightly high percentage of early failure of implants in diabetics compared to late failure. Some reports indicated increased failure rate within first year of loading signifying the risk of implant failure is associated with uncovering of implants and early stage of implant loading. The study conducted by T W Oates also supports high early failure in diabetic patients as such patients had low implant stability quotient (ISQ) in a time span of 2-12 weeks. It was also noted that, lower the level of glycemic control, higher the amount of ISQ reduction and longer the length of recovery in ISQ at base level was required. Nevertheless, most of implants attained base level of stability within 4 months even in uncontrolled diabetic patients, if the patients were refrained with micro- and macro-vascular complications.

It was observed in one study that the duration of diabetes significantly affected the success of dental implant. While another study did not demonstrate significantly higher late implant failures in diabetic patients even with longer duration.

Overall lower success of implant in patients with diabetes of extended duration may be due to increased chance of micro-vascular complications that consequently lead to deferred healing around implants and hence higher early failure.

Few studies, demonstrated significantly higher failure of implant in type-1 diabetic patients than patients with type-2 diabetes. It may be due to depletion of insulin in tissues whereas presence of insulin in tissues of type-2 diabetic individuals may reduce deleterious effect of hyperglycemia.

Immediate loading did not significantly affect the existence of dental implant in diabetic patients provided their plasma glucose level were under normal range. Balshi SF conveyed 100% survival of 18 implants after 2.5 years after placement followed by immediate loading with screwed retained fixed prosthesis in a 71-year-old diabetic patient. The study proposes that measured mechanical stimuli over implant can be advantageous for osseointegration and implant survival.

Techniques for improving success of dental implant in diabetic patients

Preoperative and post-operative, good glycemic control is mandatory to achieve improved osseointegration in diabetics. Prophylactic antibiotics have shown to be effective for success of dental implants in diabetic patients. Use of 0. 12% chlorhexidine further improves the success rate.

Few factors like implant surface characteristics (implant coated with bioactive material) and increased implant length and width has been shown to increase success rate of implant in diabetic patients.

Conclusion

The survival of dental implant in fairly controlled diabetic patients looks as good as in overall population. Use of prophylactic antibiotic, longer duration of post-surgical antibiotic course, chlorhexidine mouth rinse, implants coated with bioactive material and implant with increased width and length appears to further improve the survival of implant in diabetic individuals.

Reference:

Rajendra Kumar Dubey, Deepesh Kumar Gupta, and Amit Kumar Singh Natl J Maxillofac Surg. 2013 Jul-Dec; 4(2): 142–150.

doi: 10.4103/0975-5950.127642

Five reasons you should take an implant supported prosthesis!

People often ask me; can I get a fixed artificial teeth? While most of the time, they can get it, but in few unfortunate one, it remained impossible to provide a fixed partial denture due to their unfavorable oral conditions. In those cases, we suggest them, "you should take an implant supported prosthesis".

We see a sigh of relief on patients face. At least there is something that will solve my problem, the patient says or thinks something like this. Once they confirm the willingness for an implant supported prosthesis, it becomes a "dentist's" duty to explain its advantage.

Lest us talk about advantage and indications of implant supported prosthesis.

Improved function:

Compared to conventional removable partial dentures, the implant supported prosthesis gives a much better masticatory performance. The force, a patient can apply through implant supported teeth on food is equivalent to the natural dentition. The better chewing of food will have great positive effect on digestion and psychological overall wellbeing. It will also improve the satisfaction as the patient will be able to eat variety of food, which was limited due to poor performance of RPD.

Improved aesthetics:

The aesthetics rendered by implant supported prosthesis are greatly improved due to better emergence profile in anterior segment of the oral cavity. The ridge augmentation and other allied techniques have given ample toot to restorative dentists to help patient aesthetically.

Improved stability and support:

Implant supported dentures are as stable as natural dentition. Additional implants can be surgically placed as per the need of the support.

Conservative in nature:

The prosthesis supported by implants are conservative to soft and hard tissues. The presence of implant reduces the bone loss and maintain the soft tissue contour at the site as opposed to with a RPD. It also prevents the natural tissue loss that occurs during tooth preparation for crown and bridge.

Prevention of caries:

A tooth having crown over a natural tooth may get recurrent caries or root caries but an implant is immune for the same. Therefore, an implant supported bridge will never have a chance of secondary or root caries.

Thus, we see that the implant supported artificial teeth are the most predictable and highly satisfactory option to restore missing teeth.

Basic terminology in implant dentistry

Osseointegration

A direct structural and functional connection between ordered, living bone and the surface of a load-carrying implant 1.

Endosseous dental implant

A device inserted into the jaw bone (endosseous) to support a dental prosthesis. It is the ‘tooth root’ analogue and is often referred to as a ‘fixture’ 2.

Implant abutment

The component which attaches to the dental implant and supports the prosthesis. A transmucosal abutment (TMA) is one which passes through the mucosa overlying the implant. A temporary or healing abutment may be used during the healing of the peri-implant soft tissue before the definitive abutment is chosen 2.

Abutment screw

A screw used to connect an abutment to the implant 2.

Single stage implant surgery

Surgical placement of a dental implant which is left exposed to the oral cavity following insertion. This is the protocol used in non-submerged implant systems 2.

Two stage implant surgery

Initial surgical placement of a dental implant which is buried beneath the mucosa and then subsequently exposed with a second surgical procedure some months later. This is used in submerged implant systems 2.

Ref:

1. Albrektsson et al. Acta Orthopaedica Scand 1981.
2. Richard Palmer, Introduction to dental implants BDJ, vol 187, No. 3, Aug 14.

Postoperative bleeding, Reactionary and Secondary Haemorrhage

When you have closed an operation wound, there may start postoperative bleeding, reactionary and secondary haemorrhage. The type and reasons may be as follows:

Reactionary Haemorrage:

It occurs during the first 48 hours of the surgery. It may be due to a dislodged clot in a vessel, or a ligature has slipped.

Secondary Haemorrhage:

It occurs after 8 to 14 days after surgery. When the wound becomes infected and erodes a vessel. It may usually be quite a small one, but sometimes a larger one. One of the purposes of monitoring a patient immediately after an operation is to watch for reactionary haemorrhage, so make sure your staff observe him carefully, and take his pulse and blood pressure regularly.

 

Management of delayed haemorrhage:

If a patient's wound bleeds, apply firm local pressure and packing. If it bleeds rapidly, There may be a chance that an artery has been injured.

Minor bleeding probably comes from subcutaneous tissues, and is unlikely to be serious. If local pressure fails to control bleeding, take the patient back to the theatre and open his wound. Remove the sutures and tie or coagulate the bleeding vessels under local anaesthesia. Make sure the patient takes antibiotics.

 

You Must Know about Two Nerve Fibers in the Pulp of A Tooth

The following nerve fibers are responsible for pain of pulpal origin:

 

A Delta Fibers:

  • Largest diameter 3 to 20 mm
  • Myelinated
  • Faster conducting up to 100 m/s
  • Responsible for localized, sharp dentinal pain

Electric pulp tester stimulates A delta fibres first because of their lower threshold.
C  Fibres:

  • Smallest diameter 0.5 to 1 mm
  • Unmylinated
  • Polymodal
  • Slow conducting 0.5 to 2 m/s
  • Responsible for dull and throbbing pain

 

Thermal, chemical or mechanical stimuli stimulate “C” fibers resulting in dull, poorly, localized and throbbing pain.
NOTE: As the intensity of stimulus is increased along with A delta fibres , some of the C fibres also get stimulated resulting in strong unpleasant sensation.

Tongue: Classification

 Tongue size: House classification

 

Class I: Tongue have normal size, development and function. There are sufficient teeth present to maintain the normal form of the tongue.

Class II: Teeth had been absent for a very long time period and caused change in the form and function of the tongue.

Class III: Excessively large tongue.

 

Wright’s classification of tongue positions

Class I: Tongue lies in the floor of the mouth with tip forward and slightly below the incisal edges of the mandibular anterior teeth. This is the Ideal position of the tongue.
Class II: The tongue is flattened and broadened but the tip is in a normal position i.e. slightly upward and slightly below the incisal edges of the mandibular anterior teeth.
Class III: The tongue is retracted and depressed into the floor of the mouth, with the tip curled upward or assimilated into the body of the tongue.

Soft Palate: Classification

The soft palate can be classified in to 3 classes. They are

  1. Class 1
  2. Class 2
  3. Class 3

Class 1 soft palate: This kind of soft palate is horizontal and shows small muscular movement. This type of palate is most favourable palate from prosthodontic point of view as it permits more tissue coverage for the posterior palatal seal.
Class 2 soft palate: This type of soft palate makes 45° angle to the hard palate. With this type of soft palate, tissue coverage for posterior palatal seal is less than that of a class 1 type.
Class 3 soft palate: This type of soft palate makes around 70° angle to the hard palate. This type of soft palate provides minimum tissue coverage for posterior palatal seal for complete denture. A ‘V’ shaped palatal vault is usually associated with a class III soft palate. The development of posterior palatal seal needs special attention to hep denture retain at its place while producing “Ah” sound.

The three type of soft palates affect the design of posterior palatal seal while constructing the maxillary complete denture as follows.

In class 1 palate, the PPS will be widest.
In class 2 palate, the PPS will be medium.
in class 3 palate, the PPS will be very narrow.